Abstract
Several infectious pathologies in humans, such as tuberculosis or SARS-CoV-2, are responsible for tissue or lung damage, requiring regeneration. The regenerative capacity of adult mammals is limited to few organs. Critical injuries of non-regenerative organs trigger a repair process that leads to a definitive architectural and functional disruption, while superficial wounds result in scar formation. Tissue lesions in mammals, commonly studied under non-infectious conditions, trigger cell death at the site of the injury, as well as the production of danger signals favouring the massive recruitment of immune cells, particularly macrophages. Macrophages are also of paramount importance in infected injuries, characterized by the presence of pathogenic microorganisms, where they must respond to both infection and tissue damage. In this review, we compare the processes implicated in the tissue repair of non-infected versus infected injuries of two organs, the skeletal muscles and the lungs, focusing on the primary role of macrophages. We discuss also the negative impact of infection on the macrophage responses and the possible routes of investigation for new regenerative therapies to improve the recovery state as seen with COVID-19 patients.
Highlights
Most mammals, such as mice and humans, possess limited regenerative capacities
Elucidation of the regeneration mechanisms related to embryos and adult mammals still requires extensive studies in order to propose and develop novel therapies aimed at restoring tissues and organs in humans
Acid-induced injury triggers the rapid recruitment of neutrophils and blood-monocyte-derived MФ and the release of microparticles within the bronchoalveolar lavage fluid (BALF)
Summary
Most mammals, such as mice and humans, possess limited regenerative capacities. Only a few rare tissues or organs such as muscle, lung epithelium and liver can regenerate in adult mammals after ablation or injury, leading to an integrated morphological and functional structure. Non-infected injuries include the generation of pathogen-free lesions, such as sterile amputation, burn, freezing, crushing or drug toxicity [4,5,6] In this context, many key mechanisms for the regeneration of tissues and organs have been identified, including cell death at the site of the injury as well as danger signals, favouring massive recruitment of the immune cells, including macrophages (MФ). Non-infected injuries are as diverse as the organs they can affect: burn, crush, cut, drug exposure Despite their vast intrinsic nature, all injuries induce the same course of events that include wound closure, recruitment of immune cells and an acute inflammation phase, death of the damaged cells followed by resolution of the inflammation, cell de-differentiation and proliferation, disappearance of immune cells and formation of a novel tissue/organ [7]. While the role of the innate and adaptive immune response in resolving inflammation and regeneration has been extensively described, we will mainly focus on the innate immune response, and on MФ, in these processes
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