The human gut houses a diverse and dynamic microbiome critical for digestion, metabolism, and immune development, exerting profound efects on human health. However, these microorganisms pose a potential threat by breaching the gut barrier, entering host tissues, and triggering infections, uncontrolled infammation, and even sepsis. The intestinal epithelial cells form the primary defense, acting as a frontline barrier against microbial invasion. Antimicrobial proteins (AMPs), produced by these cells, serve as innate immune efectors that regulate the gut microbiome by directly killing or inhibiting microbes. Abnormal AMP production, whether insufcient or excessive, can disturb the microbiome equilibrium, contributing to various intestinal diseases. This review delves into the complex interactions between AMPs and the gut microbiota and sheds light on the role of AMPs in governing host-microbiota interactions. We discuss the function and mechanisms of action of AMPs, their regulation by the gut microbiota, microbial evasion strategies, and the consequences of AMP dysregulation in disease. Understanding these complex interactions between AMPs and the gut microbiota is crucial for developing strategies to enhance immune responses and combat infections within the gut microbiota. Ongoing research continues to uncover novel aspects of this intricate relationship, deepening our understanding of the factors shaping gut health. This knowledge has the potential to revolutionize therapeutic interventions, ofering enhanced treatments for a wide range of gut-related diseases.
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A polyphasic taxonomic approach was used to characterize
two novel bacterial strains, HDW17AT and HDW17BT, isolated
from the intestine of the diving beetle Cybister lewisianus,
and the dark diving beetle Hydrophilus acuminatus,
respectively. Both strains were Gram-positive and facultative
anaerobic cocci forming cream-colored colonies. The isolates
grew optimally at 25°C, pH 7, in the presence of 0.3% (wt/vol)
NaCl. Phylogenetic analysis based on 16S rRNA gene sequences
and genome sequences showed that the isolates were
members of the genus Vagococcus, and strain HDW17AT was
closely related to Vagococcus fessus CCUG 41755T (98.9% of
16S rRNA gene sequence similarity and 74.3% of average
nucleotide identity [ANI]), whereas strain HDW17BT was
closely related to Vagococcus fluvialis NCFB 2497T (98.9% of
16S rRNA gene sequence similarity and 76.6% of ANI). Both
strains contained C16:0, and C18:1 ω9c as the major cellular fatty
acids, but C16:1 ω9c was also observed only in strain HDW17BT
as the major cellular fatty acid. The respiratory quinone of the
isolates was MK-7. The major polar lipid components were
phosphatidylglycerol, phosphatidylethanolamine, and diphosphatidylglycerol.
The genomic DNA G + C content of strains
HDW17AT and HDW17BT were 36.6 and 34.4%, respectively.
Both strains had cell wall peptidoglycan composed of the
amino acids L-alanine, glycine, D-glutamic acid, L-tryptophan,
L-lysine, and L-aspartic acid, and the sugars ribose, glucose,
and galactose. Based on phylogenetic, phenotypic, chemotaxonomic,
and genotypic analyses, strains HDW17AT and
HDW17BT represent two novel species in the genus Vagococcus.
We propose the name Vagococcus coleopterorum sp.
nov. for strain HDW17AT (= KACC 21348T = KCTC 49324T
= JCM 33674T) and the name Vagococcus hydrophili sp. nov.
for strain HDW17BT (= KACC 21349T = KCTC 49325T =
JCM 33675T).
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considered a tumor-suppressor gene, it was recently
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suggesting an immunomodulatory function of PTEN in the
gut. However, this alternative function of PTEN has not yet
been evaluated in an in vivo context of protection against
enteropathogenic bacteria. To address this, we utilized IECrestricted
Pten knockout (PtenΔIEC/ΔIEC) and littermate Pten+/+
mice. These mice were subjected to the streptomycin-pretreated
mouse model of Salmonella infection, and subsequently
given an oral gavage of a low inoculum (2 × 104 CFU)
of Salmonella enterica serovar Typhimurium (S. Typhimurium).
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of PtenΔIEC/ΔIEC mice compared to Pten+/+ mice, but
also induced deleterious gastrointestinal inflammation in
PtenΔIEC/ΔIEC mice manifested by massive histological damage
to the intestinal mucosa. S. Typhimurium infection upregulated
pro-inflammatory cytokine production in the intestine
of PtenΔIEC/ΔIEC mice compared to controls. Furthermore,
bacterial loads were greatly increased in the liver,
mesenteric lymph node, and spleen of PtenΔIEC/ΔIEC mice
compared to controls. Together, these results suggest that
IEC-restricted Pten deficiency renders the host greatly susceptible
to Salmonella infection and support an immuneregulatory
role of PTEN in the gut.
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