Resistin, a cysteine-rich protein, expressed in adipocytes, was initially proposed as a link between obesity and diabetes in mice. In humans, resistin is considered to be a pro-inflammatory molecule expressed in immune cells, which plays a regulatory role in many chronic inflammatory diseases, metabolic diseases, infectious diseases, and cancers. However, increasing evidence shows that resistin functions as a host defense peptide of innate immunity, in terms of its wide-spectrum anti-microbial activity, modulation of immunity, and limitation of microbial product-induced inflammation. To date, the understanding of resistin participating in host defense mechanism is still limited. The review aims to summarize current knowledge about the biological properties, functions, and related mechanisms of resistin in host defense, which provides new insights into the pleiotropic biological function of resistin and yields promising strategies for developing new antimicrobial therapeutic agents.

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It is widely accepted that maintenance of microbial diversity is essential for the health of the respiratory tract; however, there are limited reports on the correlation between starvation and respiratory tract microbial diversity. In the present study, saline/β-hydroxybutyric acid (BHBA) intravenous injection after dietary restriction was used to imitate different degrees of starvation. A total of 13 healthy male yaks were imposed to different dietary restrictions and intravenous injections, and their nasopharyngeal microbiota profiles were obtained by metagenomic shotgun sequencing. In healthy yaks, the main dominant phyla were Proteobacteria (33.0%), Firmicutes (22.6%), Bacteroidetes (17.2%), and Actinobacteria (13.2%); the most dominated species was Clostridium botulinum (10.8%). It was found that 9 days of dietary restriction and 2 days of BHBA injection (imitating severe starvation) significantly decreased the microbial diversity and disturbed its structure and functional composition, which increased the risk of respiratory diseases. This study also implied that oral bacteria played an important role in maintaining nasopharynx microbial homeostasis. In this study, the correlation between starvation and nasopharynx microbial diversity and its potential mechanism was investigated for the first time, providing new ideas for the prevention of respiratory diseases.

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Obese mice exhibited more lymphocytes in the bronchoalveolar lavage fluid and milder lung injury after Escherichia coli (E. coli) infection. However, it remained unclear whether the spleen contributed to the effect of obese mice with infection. The study was purposed to reveal the histopathological changes of the spleen caused by oxidative stress and inflammation in diet-induced obesity (DIO) mice challenged by Escherichia coli. After infection, the spleen tissues were obtained in normal and DIO mice at 0 h (uninfected), 12 h, 24 h, and 72 h postinfection. Results revealed that DIO mice have higher contents of resistin, TNF-α, IL-6, and IL-1β in the spleen than normal mice and lower concentrations of GSH-Px, SOD, and CAT and higher MDA than normal mice. After an intranasal drip of E. coli, the activities of GSH-Px, SOD, and CAT in the DIO mice were elevated and the content of MDA declined. The activities of SOD and CAT in the normal mice declined, and the content of MDA was elevated. Moreover, the contents of TNF-α, IL-6, and IL-1β in the spleen declined in DIO mice at 24 and 72 h, although the contents of leptin, resistin, TNF-α, IL-6, and IL-1β were elevated at 12 h. The contents of resistin, TNF-α, IL-6, and IL-1β were elevated in normal mice at 12 and 24 h. Those results indicated that obesity elevated splenic oxidation and inflammatory levels, but it enhanced antioxidant capacity and reduced cytokine levels of the spleen in mice to resist splenic injury after an intranasal drip of E. coli.