Details
| Original language | English |
|---|---|
| Pages (from-to) | 96-111 |
| Number of pages | 16 |
| Journal | Exercise immunology review |
| Volume | 25 |
| Publication status | Published - 2019 |
Abstract
Many lifestyle-related diseases, such as obesity and cigarette smoke-induced pulmonary diseases, are associated with chronic systemic inflammation, which has been shown to contribute to the disease initiation and progression, and also for co-morbidities of these diseases. While the source of inflammation in obese subjects is suggested to be mainly the visceral adipose tissue, smoke-induced inflammation originates in the pulmonary system. Here, chronic cigarette smoking induces oxidative stress, resulting in severe cellular damage. During obesity, metabolic stress pathways in adipocytes induce inflammatory cascades which are also accompanied by fibrotic processes and insulin resistance. In both diseases, local inflammatory signals induce progressive immune cell infiltration, release of cytokines and a subsequent spill-over of inflammation to the systemic circulation. Exercise training represents an effective therapeutic and immune regulating strategy for both obese patients, as well as for patients with smoke induced pulmonary inflammation. While the immuneregulating impact of exercise might primarily depend on the disease state, patients with pulmonary inflammation seem to be less responsive to exercise therapy. The current review tries to identify similarities and differences between inflammatory processes, and the consequences for the immunoregulatory effects of exercise as a therapeutic agent.
Keywords
- adipose tissue, cigarette smoking, cytokines, immune system, physical activity
ASJC Scopus subject areas
- Immunology and Microbiology(all)
- Immunology
Sustainable Development Goals
Cite this
- Standard
- Harvard
- Apa
- Vancouver
- BibTeX
- RIS
In: Exercise immunology review, Vol. 25, 2019, p. 96-111.
Research output: Contribution to journal › Review article › Research › peer review
}
TY - JOUR
T1 - Inflammatory features of obesity and smoke exposure and the immunologic effects of exercise
AU - Batatinha, Helena Angelica Pereira
AU - Neto, Jose Cesar Rosa
AU - Krüger, K.
PY - 2019
Y1 - 2019
N2 - Many lifestyle-related diseases, such as obesity and cigarette smoke-induced pulmonary diseases, are associated with chronic systemic inflammation, which has been shown to contribute to the disease initiation and progression, and also for co-morbidities of these diseases. While the source of inflammation in obese subjects is suggested to be mainly the visceral adipose tissue, smoke-induced inflammation originates in the pulmonary system. Here, chronic cigarette smoking induces oxidative stress, resulting in severe cellular damage. During obesity, metabolic stress pathways in adipocytes induce inflammatory cascades which are also accompanied by fibrotic processes and insulin resistance. In both diseases, local inflammatory signals induce progressive immune cell infiltration, release of cytokines and a subsequent spill-over of inflammation to the systemic circulation. Exercise training represents an effective therapeutic and immune regulating strategy for both obese patients, as well as for patients with smoke induced pulmonary inflammation. While the immuneregulating impact of exercise might primarily depend on the disease state, patients with pulmonary inflammation seem to be less responsive to exercise therapy. The current review tries to identify similarities and differences between inflammatory processes, and the consequences for the immunoregulatory effects of exercise as a therapeutic agent.
AB - Many lifestyle-related diseases, such as obesity and cigarette smoke-induced pulmonary diseases, are associated with chronic systemic inflammation, which has been shown to contribute to the disease initiation and progression, and also for co-morbidities of these diseases. While the source of inflammation in obese subjects is suggested to be mainly the visceral adipose tissue, smoke-induced inflammation originates in the pulmonary system. Here, chronic cigarette smoking induces oxidative stress, resulting in severe cellular damage. During obesity, metabolic stress pathways in adipocytes induce inflammatory cascades which are also accompanied by fibrotic processes and insulin resistance. In both diseases, local inflammatory signals induce progressive immune cell infiltration, release of cytokines and a subsequent spill-over of inflammation to the systemic circulation. Exercise training represents an effective therapeutic and immune regulating strategy for both obese patients, as well as for patients with smoke induced pulmonary inflammation. While the immuneregulating impact of exercise might primarily depend on the disease state, patients with pulmonary inflammation seem to be less responsive to exercise therapy. The current review tries to identify similarities and differences between inflammatory processes, and the consequences for the immunoregulatory effects of exercise as a therapeutic agent.
KW - adipose tissue
KW - cigarette smoking
KW - cytokines
KW - immune system
KW - physical activity
UR - https://img1.wsimg.com/blobby/go/2b32b969-f24b-4b6f-8e61-5d111c218d54/EIR_25_2019.pdf
UR - http://www.scopus.com/inward/record.url?scp=85061485135&partnerID=8YFLogxK
M3 - Review article
VL - 25
SP - 96
EP - 111
JO - Exercise immunology review
JF - Exercise immunology review
SN - 1077-5552
ER -