Inflammation, immunological reaction and role of infection in pulmonary hypertension.
Inflammation underlies a wide variety of physiological and pathological processes. Acute inflammation is the initial response of the body to harmful stimuli. Chronic inflammation, by contrast, is a prolonged, dysregulated and maladaptive response that involves active inflammation, tissue destruction and attempts at tissue repair. Over the past few years, such persistent inflammation has been shown to be associated with pulmonary hypertension (PH). Substantial advances in basic and experimental science have illuminated the role of inflammation and the underlying cellular and molecular mechanisms that contribute to PH. This review summarizes the experimental and clinical evidence for inflammation in various types of PH. In addition, it assesses the current state of knowledge regarding the inducers/triggers of chronic inflammation and infection, as well as the inflammatory mediators and cells that are involved in PH. Infiltration of inflammatory cells, such as dendritic cells, macrophages, mast cells, T-lymphocytes and B-lymphocytes, in the vascular lesions and an elevation of serum/tissue concentrations of proinflammatory cytokines and chemokines and their contribution to pulmonary vascular remodelling are reported in detail. We review the data supporting the use of inflammatory markers as prognostic and predictive factors in PH. Finally, we consider how new insights into inflammation in PH may identify innovative therapeutic strategies.
Pullamsetti
S S
SS
Department of Lung Development and Remodelling, Max-Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.
Savai
R
R
Janssen
W
W
Dahal
B K
BK
Seeger
W
W
Grimminger
F
F
Ghofrani
H A
HA
Weissmann
N
N
Schermuly
R T
RT
D056704:Adaptive Immunity; D000818:Animals; D001402:B-Lymphocytes / Q000276:immunology; D003141:Communicable Diseases / Q000150:complications*; D006801:Humans; D006976:Hypertension, Pulmonary / Q000150:complications* / Q000276:immunology* / Q000503:physiopathology; D007113:Immunity, Innate; D018836:Inflammation Mediators / Q000276:immunology; D011014:Pneumonia / Q000150:complications / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology
D018836:Inflammation Mediators