Effect of surgery-induced weight loss on immune function

Moulin, Cristiane Martins; Rizzo, Luiz Vicente; Halpern, Alfredo

doi:10.1586/17474124.2.5.617

Cited by 19 publications

(15 citation statements)

References 16 publications

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Section: Biological Mechanisms Linking Abdominal Obesity To Cancermentioning

confidence: 99%

“…Moulin et al have recently shown that severely obese patients have a significantly lower natural killer (NK) cell cytotoxic activity as compared to normal individuals matched for age and gender, with lower defence against invaders such as precancerous and cancerous cells [112]. Interestingly, weight loss (26% less of initial weight) is responsible for an increase in NK cytotoxic activity after 6 months from gastric bypass surgery [112]. Lynch et al have recently shown that omental invariant NKT (iNKT) cell frequencies were lower in patients with severe obesity as compared to lean healthy subjects, thus suggesting a novel role for the omentum in immune regulation and tumor immunity [113].…”

Section: Biological Mechanisms Linking Abdominal Obesity To Cancermentioning

confidence: 99%

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Obesity as a Major Risk Factor for Cancer

2013

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The number of cancer cases caused by being obese is estimated to be 20% with the increased risk of malignancies being influenced by diet, weight change, and body fat distribution together with physical activity. Reports from the International Agency for Research into Cancer and the World Cancer Research Fund (WCRF) have shown that the strongest evidence exists for an association of obesity with the following cancer types: endometrial, esophageal adenocarcinoma, colorectal, postmenopausal breast, prostate, and renal, whereas the less common malignancies are leukemia, non-Hodgkin's lymphoma, multiple myeloma, malignant melanoma, and thyroid tumours. To be able to develop novel methods in prevention and treatment, we first must understand the underlying processes which link cancer to obesity. Four main systems have been identified as potential producers of cancer in obesity: insulin, insulin-like growth factor-I, sex steroids, and adipokines. Various novel candidate mechanisms have been proposed: chronic inflammation, oxidative stress, crosstalk between tumour cells and surrounding adipocytes, migrating adipose stromal cells, obesity-induced hypoxia, shared genetic susceptibility, and the functional defeat of immune function. Herein, we review the major pathogenic links between obesity and susceptibility to cancer.

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Section: Biological Mechanisms Linking Abdominal Obesity To Cancermentioning

confidence: 99%

Section: Biological Mechanisms Linking Abdominal Obesity To Cancermentioning

confidence: 99%

Obesity as a Major Risk Factor for Cancer

2013

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“…The underlying biological mechanisms still remain unclear, but there are several studies focusing on the link between obesity and cancer. Besides reduced insulin resistance [4], physical activity [5] and sex hormones [6], also the influence of obesity on immune functions is discussed [7]. Previous studies could show a central role of the adipocytokine leptin on the innate immune system [8–11].…”

Section: Introductionmentioning

confidence: 99%

“…Additionally, obese patients who lost body weight by bariatric surgery or by exercise training and nutrition courses could reverse their impaired NK cell activity and NK cell-mediated cytokine synthesis [7, 18]. This indicates that there might be a close interaction between impaired NK cell functions in obese individuals and the increased risk for cancer in obesity.…”

Section: Introductionmentioning

confidence: 99%

Significantly enhanced lung metastasis and reduced organ NK cell functions in diet-induced obese rats

et al. 2017

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BackgroundObesity was identified as a major risk factor for malignant diseases, but underlying mechanisms remain unclear. Natural killer (NK) cells, a pivotal aspect of innate immunity, are capable of identifying and killing virally infected and tumor cells. Previous studies have shown altered NK cell functions in obesity, and the current study aimed to investigate the relationship between altered NK cell functions and increased cancer risk in obesity.MethodsTo induce obesity male F344-rats received a high-fat diet (34% fat) or a control diet (4% fat). Thereafter, syngeneic mammary adenocarcinoma cells (MADB106) or a vehicle were intravenously (i.v.) injected. 15 min after injection, half of each group of rats were killed, lungs removed and immunohistochemically stained. Numbers of NK cells, MADB106 cells and NK cell-tumor cell interactions were quantified. Twenty-one days after tumor-cell injection the other half group of rats was killed and lung metastases were counted and relative mRNA concentrations of different NK cell receptors were determined.ResultsAfter short-term MADB106-challenge, DIO fed animals showed significantly decreased NK cell numbers in the blood and NK cell-tumor cell interactions in the lung as compared to their control littermates. Twenty-one days after MADB106 injection, the lungs of the DIO fed rats showed significantly more lung metastases compared to control animals, accompanied by reduced relative mRNA concentrations of the activating NK cell receptor NKG2D.ConclusionsWe conclude that induction of obesity in F344-rats leads to reduced lung NK cell function against tumor cells and results in significantly enhanced lung metastasis as compared to lean animals. It can be hypothesized that obesity-induced altered NK cell functions play an important role in cancer growth and metastasis.Electronic supplementary materialThe online version of this article (doi:10.1186/s40608-017-0161-5) contains supplementary material, which is available to authorized users.

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“…In another study, levels of monocyte chemoattractant protein-1 and interferon gamma, which are important components of the immune response to infectious pathogens, were restored after weight loss induced by RYGB [12]. Furthermore, natural killer cell activity, innate immune cells involved in the control of cancer and infections, was enhanced after RYGB [13]. Recently, an inverse relationship between the change in certain T cells (CD4+ and CD3+) and the amount of weight lost after gastric bypass surgery has been noted [14].…”

Section: Case Presentationmentioning

confidence: 99%

Histiocytic necrotizing lymphadenitis (Kikuchi-Fujimoto disease) after laparoscopic Roux-en-Y gastric bypass for morbid obesity: a case report

et al. 2012

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IntroductionKikuchi-Fujimoto disease, or histiocytic necrotizing lymphadenitis, is a rare, benign, autoimmune condition characterized by lymphadenopathy, fever and neutropenia. It is a self-limited condition of unknown etiology.Case presentationWe report the case of a 45-year-old Caucasian man with the first known case of Kikuchi disease associated with dramatic weight loss after bariatric surgery.ConclusionAlthough the association between Kikuchi disease and bariatric surgery may be entirely coincidental, we speculate whether the immune dysfunction associated with weight loss may have played an etiologic role in this process.

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Effect of surgery-induced weight loss on immune function

Abstract: The biological mechanisms that link obesity to many forms of cancer seem to be multifactorial and involve a network of metabolic and immuno logical factors."

Cited by 19 publications

References 16 publications

Obesity as a Major Risk Factor for Cancer

Obesity as a Major Risk Factor for Cancer

Significantly enhanced lung metastasis and reduced organ NK cell functions in diet-induced obese rats

Histiocytic necrotizing lymphadenitis (Kikuchi-Fujimoto disease) after laparoscopic Roux-en-Y gastric bypass for morbid obesity: a case report

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