The mechanisms mediated by α7 acetylcholine nicotinic receptors may contribute to peripheral nerve regeneration

Due to the microenvironment created by Schwann cell (SC) activity, peripheral nerve fibers are able to regenerate. Inflammation is the first response to nerve damage and the removal of cellular and myelin debris is essential in preventing the persistence of the local inflammation that may negatively affect nerve regeneration. Acetylcholine (ACh) is one of the neurotransmitters involved in the modulation of inflammation through the activity of its receptors, belonging to both the muscarinic and nicotinic classes. In this report, we evaluated the expression of α7 nicotinic acetylcholine receptors (nAChRs) in rat sciatic nerve, particularly in SCs, after peripheral nerve injury. α7 nAChRs are absent in sciatic nerve immediately after dissection, but their expression is significantly enhanced in SCs after 24 h in cultured sciatic nerve segments or in the presence of the proinflammatory neuropeptide Bradykinin (BK). Moreover, we found that activation of α7 nAChRs with the selective partial agonist ICH3 causes a decreased expression of c-Jun and an upregulation of uPA, MMP2 and MMP9 activity. In addition, ICH3 treatment inhibits IL-6 transcript level expression as well as the cytokine release. These results suggest that ACh, probably released from regenerating axons or by SC themselves, may actively promote through α7 nAChRs activation an anti-inflammatory microenvironment that contributes to better improving the peripheral nerve regeneration

Boxing injury epidemiology in Italy: a series report collected from 2016 to 2022

BACKGROUND: Boxing is an ancient sport practiced as amateur or professional activity. Recent changes in amateur boxing rules seemed to make these two sports more similar regarding the injury profile. Aim of this study was to com-pare the injury rate in amateur and professional boxing after the rules' change.METHODS: From September 2016 to June 2022, two of the authors recorded all medical conditions occurred during male boxing activity while overseeing the medical assistance of boxing events. The total number of boxing matches (and boxers) during the events was recorded. In case of a medical condition, age and body weight of the athlete were collected as well as if he was competing in amateur or professional boxing. Data related to the type of injury, treat-ment, hospital referral, other investigations, final diagnosis and boxing decision were recorded.RESULTS: In 60 months, 75 medical conditions were recorded in 36 boxing events and 349 matches (698 boxers, 54% amateur). The mean body weight of injured boxers was 68.7 +/- 9.5 kg, with no difference in respect to non-injured boxers (68.6 +/- 9.2 kg). No difference in injury rate was met when comparing different weight divisions. No major trauma was observed. Among different injury rate parameters, only the injury rate per 100 athletes proved to be higher in professional (20.19) than amateur (9.06) boxers (odd ratio 2.54). Facial wounds were the most prevalent injury, with no difference between amateur (11) and professional (4) boxers.CONCLUSIONS: Comparing amateur and professional boxing, our study showed a higher injury rate per 100 athletes in professional boxers, even if all other injury rate exposure parameters resulted not different. When an injury oc-curred, the kind of verdict and the type of injury were not different between amateur and professional boxing

The IL-17A-neutrophil axis promotes epithelial cell IL-33 production during nematode lung migration

The early migratory phase of pulmonary helminth infections is characterized by tissue injury leading to the release of the alarmin IL-33 and subsequent induction of type 2 immune responses. We recently described a role for IL-17A, through suppression of IFNγ, as an important inducer of type 2 responses during infection with the lung-migrating rodent nematode Nippostrongylus brasiliensis. Here, we aimed to investigate the interaction between IL-17A and IL-33 during the early lung migratory stages of N. brasiliensis infection. In this brief report, we demonstrate that deficiency of IL-17A leads to impaired IL-33 expression and secretion early in infection, independent of IL-17A suppression of IFNγ. Neutrophil-depletion experiments, which dramatically reduce lung injury, revealed that neutrophils are primarily responsible for the IL-17A-dependent release of IL-33 into the airways. Taken together, our results reveal an IL-17A-neutrophil-axis that can drive IL-33 during helminth infection, highlighting an additional pathway by which IL-17A regulates pulmonary type 2 immunity.</p