Chronic Inflammation: Cause (Low Cell O2) and Solutions

Medical people Chronic inflammation, on a cell level, has a single cause. Among the key driving forces of chronic inflammation, according to recent research studies, are pro-inflammatory transcription factors, such as nuclear factor kappa B (NF-kappaB), activator protein (AP)-1 (Safronova & Morita, 2010; Ryan et al, 2009), and hypoxia-inducible factor 1 (Imtiyaz & Simon, 2010; Sumbayev & Nicholas, 2010). Chronic diseases, as it has been known for decades, are also based on cell hypoxia.

New discoveries in medicine suggest that in order to reduce chronic inflammation we need to breathe slower and less 24/7. Why is it so? We need more oxygen in tissues and chronic diseases and chronic inflammation, according to recent biomedical research, is either associated with or even caused by tissue hypoxia (reduced oxygen level in body cells). Medical biologists have finally been able to pinpoint the mechanism.

Sick people with chronic inflammation Both effects, chronic inflammation and low oxygen levels in cells, are common in people with chronic diseases, such as:
- arthritic conditions
- Alzheimer's disease
- asthma
- autoimmune diseases
- acne
- allergic reactions
- atherosclerosis
- chronic prostatitis
- Crohn's disease
- COPD
- dermatitis
- hepatitis
- hypersensitivities and allergic reactions
- insulin resistance (diabetes) MDs and patients
- irritable bowel syndrome (IBS) of the intestinal tract
- inflammatory bowel diseases (IBD)
- lupus
- nephritis
- obesity
- cachexia
- gastrointestinal ischemia
- osteoarthritis
- pelvic inflammatory disease
- Parkinson's disease
- sarcoidosis
- sleep apnea
- transplant rejection
- and ulcerative colitis.

Symptoms of these chronic diseases include inflammation and other related effects.

Several other chronic diseases (including cancer, atherosclerosis, and ischemic heart disease) have their origins in chronic inflammatory processes.

Why is chronic inflammation common in people with chronic diseases?

Minute ventilation rates (chronic diseases)

Condition	Minute ventilation	Number of people	All references or click below for abstracts
Normal breathing	6 L/min	-	Medical textbooks
Healthy Subjects	6-7 L/min	>400	Results of 14 studies
Heart disease	15 (±4) L/min	22	Dimopoulou et al, 2001
Heart disease	16 (±2) L/min	11	Johnson et al, 2000
Heart disease	12 (±3) L/min	132	Fanfulla et al, 1998
Heart disease	15 (±4) L/min	55	Clark et al, 1997
Heart disease	13 (±4) L/min	15	Banning et al, 1995
Heart disease	15 (±4) L/min	88	Clark et al, 1995
Heart disease	14 (±2) L/min	30	Buller et al, 1990
Heart disease	16 (±6) L/min	20	Elborn et al, 1990
Pulm hypertension	12 (±2) L/min	11	D'Alonzo et al, 1987
Cancer	12 (±2) L/min	40	Travers et al, 2008
Diabetes	12-17 L/min	26	Bottini et al, 2003
Diabetes	15 (±2) L/min	45	Tantucci et al, 2001
Diabetes	12 (±2) L/min	8	Mancini et al, 1999
Diabetes	10-20 L/min	28	Tantucci et al, 1997
Diabetes	13 (±2) L/min	20	Tantucci et al, 1996
Asthma	13 (±2) L/min	16	Chalupa et al, 2004
Asthma	15 L/min	8	Johnson et al, 1995
Asthma	14 (±6) L/min	39	Bowler et al, 1998
Asthma	13 (±4) L/min	17	Kassabian et al, 1982
Asthma	12 L/min	101	McFadden & Lyons, 1968
COPD	14 (±2) L/min	12	Palange et al, 2001
COPD	12 (±2) L/min	10	Sinderby et al, 2001
COPD	14 L/min	3	Stulbarg et al, 2001
Sleep apnea	15 (±3) L/min	20	Radwan et al, 2001
Liver cirrhosis	11-18 L/min	24	Epstein et al, 1998
Hyperthyroidism	15 (±1) L/min	42	Kahaly, 1998
Cystic fibrosis	15 L/min	15	Fauroux et al, 2006
Cystic fibrosis	10 L/min	11	Browning et al, 1990
Cystic fibrosis*	10 L/min	10	Ward et al, 1999
CF and diabetes*	10 L/min	7	Ward et al, 1999
Cystic fibrosis	16 L/min	7	Dodd et al, 2006
Cystic fibrosis	18 L/min	9	McKone et al, 2005
Cystic fibrosis*	13 (±2) L/min	10	Bell et al, 1996
Cystic fibrosis	11-14 L/min	6	Tepper et al, 1983
Epilepsy	13 L/min	12	Esquivel et al, 1991
CHV	13 (±2) L/min	134	Han et al, 1997
Panic disorder	12 (±5) L/min	12	Pain et al, 1991
Bipolar disorder	11 (±2) L/min	16	MacKinnon et al, 2007
Dystrophia myotonica	16 (±4) L/min	12	Clague et al, 1994

Hyperventilation (or breathing more than the medical norms) is the main cause of chronic inflammation in modern people. Let us consider the mechanism. Alveolar hypocapnia caused by chronic hyperventilation (overbreathing) leads to low oxygen tension in the heart, brain, stomach, intestinal tract, kidneys, liver, joints, and systemic body hypoxia. (When we hyperventilate, we have less oxygen in the body - see the Web page CO2: Cells Oxygen Supplier with numerous medical quotes and references, as well as CO2-O2 Transport).

Chronic Inflammation Treatment

Hence, restoration of normal breathing parameters is the main treatment required to gradually increase body oxygen levels (see the CP test below) and then reduce and eliminate symptoms of chronic inflammation, while other therapies and measures have their additional value. Furthermore, prevention and avoidance of allergic reactions, if any, is necessary for clinical remission of chronic inflammation. Upon achievement of about 35-40 s for the morning CP - body oxygen test (this corresponds to the medical norm for breathing), different types of chronic inflammation disappear within 2-3 weeks. This is true for gastritis, sinusitis, pancreatitis, duodenitis, hepatitis, arthritis, problems with liver, and many others conditions. Furthermore, Russian Buteyko breathing doctors had a successful clinical trial on patients with liver cirrhosis and hepatitis B, while thousands of their patients solved problems with chronic inflammation using breathing retraining.

Reference Web Pages: Breathing norms, Medical Graphs and Tables about Breathing Rates (Minute Ventilation) and Body Oxygen in Healthy, Normal and Sick People
Breathing norms Parameters, graph, and description of the normal breathing pattern
6 breathing myths 6 myths about breathing and body oxygenation (prevalence: over 90%)
Hyperventilation Definitions of hyperventilation: their advantages and weak points
Hyperventilation Syndrome in the Sick. Table 1. Western scientific evidence about prevalence of CHV (chronic hyperventilation) in patients with various chronic conditions (34 medical studies)
Normal Minute Ventilation in Healthy Subjects: Easy and Light Breathing (14 Studies)
Hyperventilation Prevalence Present in Over 90% of Normal People (24 medical publications)
HV and hypoxia How and why deep breathing reduces oxygenation of cells and tissues of all vital organs
Body oxygen test How to measure your own breathing and body oxygenation (a simple DIY test)
Body oxygen in healthy Table 4. CP (body oxygen level) in healthy people (27 medical studies)
Body oxygen in sick Table 5. CP (body oxygen level) in sick people (14 medical studies)
Buteyko Table of Health Zones with clinical description of most common zones
Morning HV Morning hyperventilation effect or how and why critically ill people are most likely to die during early morning hours

References: CO2 Effects Web Pages
Vasodilation: CO2 expands arteries and arterioles facilitating perfusion (or blood supply) to all vital organs
The Bohr effect How and why oxygen is released by red blood cells in tissues
Cell Oxygen Levels and oxygen transport are controlled by alveolar CO2 and breathing
Oxygen Transport depends on breathing and these two effects (Vasoconstriction-Vasodilation and the Bohr effect) are parts of two diagrams that summarize influences of hypocapnia (low CO2 content in the blood and cells) on circulation and O2 delivery
Free Radical Generation takes place due to anaerobic cell respiration caused by cell hypoxia. Hence, antioxidant defenses of the human body are also regulated by CO2 and breathing
Inflammatory Response is controlled by breathing since hypoxia leads to or intensifies chronic inflammation through over-expression of the hypoxia-inducible factor 1, while normal breathing reduces these processes
Nerve stabilization takes place due to calmative or sedative effects of carbon dioxide in neurons or nerve cells
Muscle relaxation or relaxation of muscle cells is normal at high CO2, while hypocapnia causes muscular tension, poor posture and, sometimes, aggression and violence
Brochodilation - dilation of airways (bronchi and bronchioles) by carbon dioxide, and their constriction due to hypocapnia
Blood pH regulation and regulation of other bodily fluids
CO2: Lung Damage Healer: Elevated carbon dioxide prevents injury and promotes healing of lung tissues
CO2: Skin and Tissue Healer
Synthesis of Glutamine in the Brain, CO2 fixation, and other chemical reactions
CO2 myth "CO2 is a toxic waste gas" myth
Breathing control How is our breathing regulated? Why hypocapnia makes breathing uneven and erratic

References

Lancet. 1999 Oct 9;354(9186):1283-6.
Carbon dioxide and the critically ill--too little of a good thing?
Laffey JG, Kavanagh BP.
Department of Anaesthesia and Medical-Surgical Intensive Care Unit, Toronto General Hospital, University Health Network, University of Toronto, Ontario, Canada.
Permissive hypercapnia (acceptance of raised concentrations of carbon dioxide in mechanically ventilated patients) may be associated with increased survival as a result of less ventilator-associated lung injury. Conversely, hypocapnia is associated with many acute illnesses (eg, asthma, systemic inflammatory response syndrome, pulmonary oedema), and is thought to reflect underlying hyperventilation. Accumulating clinical and basic scientific evidence points to an active role for carbon dioxide in organ injury, in which raised concentrations of carbon dioxide are protective, and low concentrations are injurious. We hypothesise that therapeutic hypercapnia might be tested in severely ill patients to see whether supplemental carbon dioxide could reduce the adverse effects of hypocapnia and promote the beneficial effects of hypercapnia. Such an approach could also expand our understanding of the pathogenesis of disorders in which hypocapnia is a constitutive element.

Curr Opin Organ Transplant. 2010 Aug;15(4):411-5.
Inflammation and the balance of Treg and Th17 cells in transplant rejection and tolerance.
Hanidziar D, Koulmanda M.
Transplant Institute, Department of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Ave., Boston, MA 02215, USA.
PURPOSE OF REVIEW: Inflammation of the allograft, occurring as a consequence of hypoxia and ischemia/reperfusion injury, adversely influences short-term and long-term transplant outcomes. Thus far, imbalance of tissue-protective Treg and tissue-destructive Th17 cells has been confirmed in a number of tissue-inflammatory states, including autoimmune disease. Hence, benefits of tilting Treg-Th17 equilibrium toward dominance of Tregs may promote transplant tolerance.
RECENT FINDINGS: Adverse graft inflammation creates extreme resistance to the induction of donor-specific tolerance. Proinflammatory cytokines, when abundantly expressed within the graft and draining lymph nodes, prevent commitment of donor-activated T cells into graft-protective, T-regulatory phenotype, while fostering generation of donor-reactive Th1, Th2 or Th17 effector subsets. In addition, the inflammatory milieu may destabilize the program of both natural and induced Tregs, converting them into inflammatory, effector-like phenotypes. Therefore permanent, Treg-dependent acceptance of an allograft may not be achieved without limiting adverse tissue inflammation.
SUMMARY: Balance of graft-protective regulatory and graft-destructive effector T cells largely depends on the balance of proinflammatory and anti-inflammatory cytokines in the milieu, in which donor-directed T-cell response occurs. In the absence of proinflammatory cytokines, the constitutive expression of TGF-beta may guide recipient T cells into a tissue-protective, pro-tolerant mode. Therefore, targeting adverse tissue inflammation may represent a powerful means to tilt antidonor immunity towards tolerance.

Curr Top Microbiol Immunol. 2010;345:105-20.
Hypoxia-inducible factors as essential regulators of inflammation.
Imtiyaz HZ, Simon MC.
Abramson Family Cancer Research Institute, University of Pennsylvania, 438 BRB II/III, 421 Curie Boulevard, Philadelphia, PA 19104-6160, USA.
Myeloid cells provide important functions in low oxygen (O(2)) environments created by pathophysiological conditions, including sites of infection, inflammation, tissue injury, and solid tumors. Hypoxia-inducible factors (HIFs) are principle regulators of hypoxic adaptation, regulating gene expression involved in glycolysis, erythropoiesis, angiogenesis, proliferation, and stem cell function under low O(2). Interestingly, increasing evidence accumulated over recent years suggests an additional important regulatory role for HIFs in inflammation. In macrophages, HIFs not only regulate glycolytic energy generation, but also optimize innate immunity, control pro-inflammatory gene expression, mediate bacterial killing and influence cell migration. In neutrophils, HIF-1a promotes survival under O(2)-deprived conditions and mediates blood vessel extravasation by modulating ß (2) integrin expression. Additionally, HIFs contribute to inflammatory functions in various other components of innate immunity, such as dendritic cells, mast cells, and epithelial cells. This review will dissect the role of each HIF isoform in myeloid cell function and discuss their impact on acute and chronic inflammatory disorders. Currently, intensive studies are being conducted to illustrate the connection between inflammation and tumorigenesis. Detailed investigation revealing interaction between microenvironmental factors such as hypoxia and immune cells is needed. We will also discuss how hypoxia and HIFs control properties of tumor-associated macrophages and their relationship to tumor formation and progression.

Arch Immunol Ther Exp (Warsz). 2010 Aug;58(4):287-94. Epub 2010 May 26.
Hypoxia-inducible factor 1 as one of the "signaling drivers" of Toll-like receptor-dependent and allergic inflammation.
Sumbayev VV, Nicholas SA.
Medway School of Pharmacy, University of Kent, Anson Building, Central Avenue,
Chatham Maritime, Kent ME44TB, UK. V.Sumbayev@kent.ac.uk
Hypoxia-inducible factor 1 (HIF-1) is a heterodimeric transcription complex which plays a crucial role in cellular adaptation to low oxygen availability. In the last years there has been increasing evidence about the role of this factor in inflammatory/innate immune reactions. It has also been found to contribute to different types of allergic inflammation.

Mediators Inflamm. 2010;2010:585989. Epub 2010 Apr 20.
Systemic inflammation in chronic obstructive pulmonary disease: may adipose tissue play a role? Review of the literature and future perspectives.
Tkacova R.
Department of Respiratory Medicine and Tuberculosis, Faculty of Medicine, P J Safarik University, L. Pasteur Teaching Hospital, Kosice, Slovakia.
Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality worldwide. Low-grade systemic inflammation is considered a hallmark of COPD that potentially links COPD to increased rate of systemic manifestations of the disease. Obesity with/without the metabolic syndrome and cachexia represent two poles of metabolic abnormalities that may relate to systemic inflammation. On one hand systemic inflammatory syndrome likely reflects inflammation in the lungs, i.e. results from lung-to plasma spillover of inflammatory mediators. On the other hand, obesity-related hypoxia results in local inflammatory response within adipose tissue per se, and may contribute to elevations in circulatory mediators by spillover from the adipose tissue to the systemic compartment. The extent to which systemic hypoxia contributes to the adipose tissue inflammation remains unknown. We assume that in patients with COPD and concurrent obesity at least three factors play a role in the systemic inflammatory syndrome: the severity of pulmonary impairment, the degree of obesity-related adipose tissue hypoxia, and the severity of systemic hypoxia due to reduced pulmonary functions. The present review summarizes the epidemiological and clinical evidence linking COPD to obesity, the role of adipose tissue as an endocrine organ, and the role of hypoxia in adipose tissue inflammation.

J Dent Res. 2010 May;89(5):430-44. Epub 2010 Mar 26.
Transcriptome remodeling in hypoxic inflammation.
Safronova O, Morita I.
Department of Cellular Physiological Chemistry, Tokyo Medical and Dental University, 1-5-45, Yushima, Bunkyo-ku, Tokyo 113-8549, Japan.
Hypoxia is an integral component of the inflamed tissue microenvironment. Today, the influence of hypoxia on the natural evolution of inflammatory responses is widely accepted; however, many molecular and cellular mechanisms mediating this relationship remain to be clarified. Hypoxic stress affects several independent transcriptional regulators related to inflammation in which HIF-1 and NF-kappaB play central roles. Transcription factors interact with both HATs and HDACs, which are components of large multiprotein co-regulatory complexes. This review summarizes the current knowledge on hypoxia-responsive transcriptional pathways in inflammation and their importance in the etiology of chronic inflammatory diseases, with the primary focus on transcriptional co-regulators and histone modifications in defining gene-specific transcriptional responses in hypoxia, and on the recent progress in the understanding of hypoxia-mediated epigenetic reprogramming. Furthermore, this review discusses the molecular cross-talk between glucocorticoid anti-inflammatory pathways and hypoxia.

Adv Exp Med Biol. 2010;662:27-32.
Alveolar hypoxia-induced systemic inflammation: what low PO(2) does and does not do.
Gonzalez NC, Wood JG.
Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, KS 66160, USA. ngonzale@kumc.edu
Reduction of alveolar PO(2) (alveolar hypoxia, AH) may occur in pulmonary diseases such as chronic obstructive pulmonary disease (COPD), or in healthy individuals ascending to altitude. Altitude illnesses may develop in non-acclimatized persons who ascend rapidly. The mechanisms underlying these illnesses are not well understood, and systemic inflammation has been suggested as a possible contributor. Similarly, there is evidence of systemic inflammation in the systemic alterations present in COPD patients, although its role as a causative factor is not clear. We have observed that AH, induced by breathing 10% O(2) produces a rapid (minutes) and widespread micro vascular inflammation in rats and mice. This inflammation has been observed directly in the mesenteric, skeletal muscle, and pial microcirculations. The inflammation is characterized by mast cell degranulation, generation of reactive O(2) species, reduced nitric oxide levels, increased leukocyte-endothelial adherence in post-capillary venules, and extravasation of albumin. Activated mast cells stimulate the renin-angiotensin system (RAS) which leads to the inflammatory response via activation of NADPH oxidase. If the animals remain in hypoxia for several days, the inflammation resolves and exposure to lower PO(2) does not elicit further inflammation, suggesting that the vascular endothelium has "acclimatized" to hypoxia. Recent experiments in cremaster microcirculation suggest that the initial trigger of the inflammation is not the reduced tissue PO(2), but rather an intermediary released by alveolar macrophages into the circulation. The putative intermediary activates mast cells, which, in turn, stimulate the local renin-angiotensin system and induce inflammation.

Expert Opin Ther Targets. 2009 Nov;13(11):1267-77.
Targeting the A2B adenosine receptor during gastrointestinal ischemia and inflammation.
Eltzschig HK, Rivera-Nieves J, Colgan SP.
University of Colorado, Mucosal Inflammation Program, Department of Medicine, Denver, 12700 E 19th Avenue, Mailstop B112, Research Complex 2, Room 7124, Aurora, CO 80045, USA. holger.eltzschig@ucdenver.edu
... In addition, we discuss the role of this pathway in dampening hypoxia-elicited inflammation, specifically in the setting of intestinal ischemia and inflammation.

Thorax. 2009 Jul;64(7):631-6.
Systemic inflammation: a key factor in the pathogenesis of cardiovascular complications in obstructive sleep apnoea syndrome?
Ryan S, Taylor CT, McNicholas WT.
Sleep Research Laboratory, St Vincent's University Hospital, Dublin, Ireland.
... Intermittent hypoxia, the hallmark of OSAS, results in activation of pro-inflammatory transcription factors such as nuclear factor kappa B (NF-kappaB) and activator protein (AP)-1. These promote activation of various inflammatory cells, particularly lymphocytes and monocytes, with the downstream consequence of expression of pro-inflammatory mediators that may lead to endothelial dysfunction. This review provides a critical analysis of the current evidence for an association between OSAS, inflammation and cardiovascular disease, discusses basic mechanisms that may be responsible for this association and proposes future research possibilities.

Respir Res. 2009 Jun 22;10:54.
Alveolar hypoxia, alveolar macrophages, and systemic inflammation.
Chao J, Wood JG, Gonzalez NC.
Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, KS 66160, USA. jchao@kumc.edu
... Evidence obtained in intact animals and in primary cell cultures indicate that alveolar macrophages activated by hypoxia release a mediators into the circulation. This mediator activates perivascular mast cells and initiates a widespread systemic inflammation. The inflammatory cascade includes activation of the local renin-angiotensin system and results in increased leukocyte-endothelial interactions in post-capillary venules, increased microvascular levels of reactive O2 species; and extravasation of albumin.

Eur Respir J. 2009 May;33(5):1195-205.
Cardiovascular disease in obstructive sleep apnoea syndrome: the role of intermittent hypoxia and inflammation.
Garvey JF, Taylor CT, McNicholas WT.
Respiratory Sleep Disorders Unit, St. Vincent's University Hospital, Dublin,
Ireland.
There is increasing evidence that intermittent hypoxia plays a role in the development of cardiovascular risk in obstructive sleep apnoea syndrome (OSAS) through the activation of inflammatory pathways....

Semin Immunopathol. 2009 Jun;31(1):113-25. Epub 2009 Apr 29.
Obstructive sleep apnea, immuno-inflammation, and atherosclerosis.
Arnaud C, Dematteis M, Pepin JL, Baguet JP, Lévy P.
INSERM ERI17, Grenoble, 38043, France.
Obstructive sleep apnea (OSA) is a highly prevalent sleep disorder leading to cardiovascular and metabolic complications. OSA is also a multicomponent disorder, with intermittent hypoxia (IH) as the main trigger for the associated cardiovascular and metabolic alterations. Indeed, recurrent pharyngeal collapses during sleep lead to repetitive sequences of hypoxia-reoxygenation. This IH (intermittent hypoxia) induces several consequences such as hemodynamic, hormonometabolic, oxidative, and immuno-inflammatory alterations that may interact and aggravate each other, resulting in artery changes, from adaptive to degenerative atherosclerotic remodeling.... Oxidative stress, inflammation, and vascular remodeling can be directly triggered by IH, further aggravated by the OSA-associated hormonometabolic alterations, such as insulin resistance, dyslipidemia, and adipokine imbalance.

Arthritis Res Ther. 2009;11(1):215. Epub 2009 Feb 23.
Hypoxia. Regulation of NFkappaB signalling during inflammation: the role of hydroxylases.
Oliver KM, Taylor CT, Cummins EP.
School of Medicine and Medical Science, Conway Institute, University College Dublin, Belfield, Dublin 4, Ireland.
... Microenvironmental hypoxia has long been identified as being coincident with chronic inflammation...

Acta Med Port. 2008 Sep-Oct;21(5):489-96. Epub 2009 Jan 16.
[The role of adipose tissue and macrophages in chronic inflammation associated with obesity: clinical implications].
[Article in Portuguese]
Ramalho R, Guimarães C.
Serviço e Laboratório de Imunologia, Faculdade de Medicina da Universidade do Porto, Porto.
... so, hypoxia can be a critical factor in inflammatory obese state manifestation...

J Physiol. 2008 Sep 1;586(Pt 17):4055-9. Epub 2008 Jul 3.
Interdependent roles for hypoxia inducible factor and nuclear factor-kappaB in hypoxic inflammation.
Taylor CT.
UCD Conway Institute, University College Dublin, Belfield, Dublin 4, Ireland.
Decreased oxygen availability (hypoxia) is a hallmark feature of the microenvironment in a number of chronic inflammatory conditions including arthritis and inflammatory bowel disease (IBD). Recent advances in our understanding of oxygen-dependent cell signaling have uncovered several mechanisms by which hypoxia impacts upon the development of inflammation through the coordinated expression of adaptive, inflammatory and apoptotic genes...

Methods Enzymol. 2007;435:405-19.
Regulation of hypoxia-inducible factors during inflammation.
Frede S, Berchner-Pfannschmidt U, Fandrey J.
Institut für Physiologie, Universität Duisburg-Essen, Essen, Germany.
The microenvironment of inflamed and injured tissue is characterized by low levels of oxygen and glucose and high levels of inflammatory cytokines, reactive oxygen, and nitrogen species and metabolites....

Proc Am Thorac Soc. 2005;2(1):26-33.
Local and systemic inflammation in chronic obstructive pulmonary disease.
Wouters EF.
Department of Pulmonary Diseases, University Hospital Maastricht, P.O. Box 5800,
6202 As Maastricht, The Netherlands
There is growing evidence for systemic inflammation in chronic obstructive pulmonary disease (COPD)... The main causes of systemic inflammation in COPD remain to be elucidated, although systemic hypoxia is a candidate factor.

Ophthalmologe. 2003 May;100(5):363-70.
[Diabetic retinopathy. Pathophysiology and therapy of hypoxia-induced inflammation].
[Article in German]
Joussen AM, Fauser S, Krohne TU, Lemmen KD, Lang GE, Kirchhof B.

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