The gut as a potential trigger of exercise-induced inflammatory responses

Marshall, John C.

doi:10.1139/y98-049

Cited by 96 publications

(35 citation statements)

References 33 publications

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“…Endotoxaemia due to increased intestinal barrier permeability during strenuous exercise has been recognised in human athletes and Thoroughbred racehorses [35,36]. The potential for bacterial translocation from the gastrointestinal tract during exercise has also been proposed [37]. Gram-positive cocci, consistent with the synovial isolates from the present study, were occasionally identified in a study of bacteraemia in horses with diarrhoea [29].…”

Section: Origins Of Bacteraemiasupporting

confidence: 67%

Synovial sepsis of unknown origin in the adult Thoroughbred racehorse

Byrne¹,

Lumsden²,

Lang³

et al. 2019

Equine Veterinary Journal

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Summary Background Synovial sepsis of unknown origin is a rare cause of lameness in the adult horse, and a haematogenous pathogenesis has been proposed in previous cases. Objectives To describe the features and outcome of synovial sepsis of unknown origin in adult Thoroughbred racehorses. Study design Retrospective case series. Methods Hospital records for admissions between 2005 and 2015 were reviewed to identify adult horses diagnosed with synovial sepsis of unknown origin. Presentation, clinicopathological, microbiological and diagnostic imaging findings were recorded. Treatment methods, surgical findings, complications and long‐term outcome were evaluated. Results Eleven cases were identified over the study period. Diagnosis was established from clinical examination and clinicopathologic findings, which were comparable to other aetiologies of synovial sepsis. Affected structures included synovial joints, tendon sheaths and bursae. Concurrent osteochondritis dissecans or articular cartilage lesions were evident during arthroscopic surgery in three cases. Significant intrasynovial haemorrhage was not identified. Microbial culture of synovial fluid or synovial biopsy was positive in 6/11 of cases, with all isolates being Gram‐positive cocci. Of the 6 positive microbial cultures, all isolates demonstrated in vitro sensitivity to a cephalosporin antimicrobial agent. A concurrent remote wound was present in a single case. No other potential origins of bacteraemia were identified. Treatment methods included endoscopic surgery, standing multineedle lavage, intravenous regional limb perfusion, intrasynovial medication and/or systemic antimicrobial administration. All horses survived to hospital discharge. For the 6/11 cases that raced following synovial sepsis, the median period for return to racing was 221 days. Main limitations A small study population, which was retrospectively reviewed. Conclusions Synovial sepsis of unknown origin is rare in the adult Thoroughbred racehorse and can affect a range of synovial structures. A concurrent potential source of bacteraemia is rarely identified. With appropriate management, the prognosis to return to racing is fair.

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Section: Origins Of Bacteraemiasupporting

confidence: 67%

Synovial sepsis of unknown origin in the adult Thoroughbred racehorse

Byrne¹,

Lumsden²,

Lang³

et al. 2019

Equine Veterinary Journal

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“…The gut has long being regarded as a ‘trigger’ or ‘promoter’ of sepsis and multiorgan failure (MOF); the important role of gut dysfunction has been illustrated in numerous studies [24-27]. Marshall aptly described the gastrointestinal tract as an ‘undrained abscess’ [28].…”

Section: Discussionmentioning

confidence: 99%

The role of intestinal mucosa injury induced by intra-abdominal hypertension in the development of abdominal compartment syndrome and multiple organ dysfunction syndrome

et al. 2013

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IntroductionAbdominal distension is common in critical illness. There is a growing recognition that intra-abdominal hypertension (IAH) may complicate nonsurgical critical illness as well as after abdominal surgery. However, the pathophysiological basis of the injury to the intestinal mucosal barrier and its influence on the onset of abdominal compartment syndrome (ACS) and multiorgan dysfunction syndrome (MODS) remain unclear. We measured intestinal microcirculatory blood flow (MBF) during periods of raised intra-abdominal pressure (IAP) and examined how this influenced intestinal permeability, systemic endotoxin release, and histopathological changes.MethodsTo test different grades of IAH to the injury of intestinal mucosa, 96 New Zealand white rabbits aged 5 to 6 months were exposed to increased IAP under nitrogen pneumoperitoneum of 15 mmHg or 25 mmHg for 2, 4 or 6 hours. MBF was measured using a laser Doppler probe placed against the jejunal mucosa through a small laparotomy. Fluorescein isothiocyanate (FITC)-conjugated dextran was administered by gavage. Intestinal injury and permeability were measured using assays for serum FITC-dextran and endotoxin, respectively, after each increase in IAP. Structural injury to the intestinal mucosa at different levels of IAH was confirmed by light and transmission electron microscopy.ResultsMBF reduced from baseline by 40% when IAP was 15 mmHg for 2 hours. This doubled to 81% when IAP was 25 mmHg for 6 hours. Each indicator of intestinal injury increased significantly, proportionately with IAP elevation and exposure time. Baseline serum FITC-dextran was 9.30 (± SD 6.00) μg/ml, rising to 46.89 (±13.43) μg/ml after 15 mmHg IAP for 4 hours (P <0.01), and 284.59 (± 45.18) μg/ml after 25 mmHg IAP for 6 hours (P <0.01). Endotoxin levels showed the same pattern. After prolonged exposure to increased IAP, microscopy showed erosion and necrosis of jejunal villi, mitochondria swelling and discontinuous intracellular tight junctions.ConclusionsIntra-abdominal hypertension can significantly reduce MBF in the intestinal mucosa, increase intestinal permeability, result in endotoxemia, and lead to irreversible damage to the mitochondria and necrosis of the gut mucosa. The dysfunction of the intestinal mucosal barrier may be one of the important initial factors responsible for the onset of ACS and MODS.

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“…Unlike psychosocial stress, exercise is accompanied by target tissue metabolic signals (e.g., profound change in pH, lactic acid, temperature, PO 2 , and PCO 2 ) that themselves can independently alter immune mediators [like heat shock proteins (38,73)] and leukocyte function (76). There is even evidence that exercise may be accompanied by translocation of gut bacteria into the central circulation, causing a classic antigen-mediated systemic immune response (18,58,85). Finally, in recent years, Pedersen, Febbraio, and their collaborators have made the groundbreaking discovery that working muscle tissue itself produces immune mediators like IL-6 and IL-8 (2,37).…”

Section: The Stress and Inflammatory Response To Exercisementioning

confidence: 99%

Dangerous exercise: lessons learned from dysregulated inflammatory responses to physical activity

Cooper¹,

Radom‐Aizik²,

Schwindt³

et al. 2007

Journal of Applied Physiology

123

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Exercise elicits an immunological "danger" type of stress and inflammatory response that, on occasion, becomes dysregulated and detrimental to health. Examples include anaphylaxis, exercise-induced asthma, overuse syndromes, and exacerbation of intercurrent illnesses. In dangerous exercise, the normal balance between pro- and anti-inflammatory responses is upset. A possible pathophysiological mechanism is characterized by the concept of exercise modulation of previously activated leukocytes. In this model, circulating leukocytes are rendered more responsive than normal to the immune stimulus of exercise. For example, in the case of exercise anaphylaxis, food-sensitized immune cells may be relatively innocuous until they are redistributed during exercise from gut-associated circulatory depots, like the spleen, into the central circulation. In the case of asthma, the prior activation of leukocytes may be the result of genetic or environmental factors. In the case of overuse syndromes, the normally short-lived neutrophil may, because of acidosis and hypoxia, inhibit apoptosis and play a role in prolongation of inflammation rather than healing. Dangerous exercise demonstrates that the stress/inflammatory response caused by physical activity is robust and sufficiently powerful, perhaps, to alter subsequent responses. These longer term effects may occur through as yet unexplored mechanisms of immune "tolerance" and/or by a training-associated reduction in the innate immune response to brief exercise. A better understanding of sometimes failed homeostatic physiological systems can lead to new insights with significant implication for clinical translation.

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The gut as a potential trigger of exercise-induced inflammatory responses

Cited by 96 publications

References 33 publications

Synovial sepsis of unknown origin in the adult Thoroughbred racehorse

Synovial sepsis of unknown origin in the adult Thoroughbred racehorse

The role of intestinal mucosa injury induced by intra-abdominal hypertension in the development of abdominal compartment syndrome and multiple organ dysfunction syndrome

Dangerous exercise: lessons learned from dysregulated inflammatory responses to physical activity

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