Abstract
The fish immune system, which consists of innate and adaptive immunologic processes, defends against viruses, bacteria, fungi, and parasites. The gut immunity is an integral part of the host immune system that controls immunological homeostasis, hosts' interactions with their microbiomes, and provides defence against a number of intestinal infections. Lepidocephalichthys guntea, a facultative air-breathing fish, was experimentally infected with Aeromonas hydrophila using intraperitoneal injection followed by bath challenge, and transcriptome data were used to examine the gut immune responses during disease progression and recovery from the diseased state without the use of medication. For the control or uninfected fish (FGC) and the infected fish that were kept for seven days (FGE1) and fifteen days (FGE2), separate water tanks were set up. Coding DNA sequences (CDS) for FGC and FGE1, FGC and FGE2, and FGE1 and FGE2 were analyzed for differential gene expression (DGE). The presence and expression of genes involved in the T cell receptor (TCR) signalling pathway, natural killer (NK) cell-mediated cytotoxicity pathway, and complement-mediated pathway, along with a large number of other immune-related proteins, and heat shock protein (HSPs) under various experimental conditions and its relationship to immune modulation of the fish gut was the primary focus of this study. Significant up-and-down regulation of these pathways shows that, in FGE1, the fish's innate immune system was engaged, whereas in FGE2, the majority of innate immune mechanisms were repressed, and adaptive immunity was activated. Expression of genes related to the immune system and heat-shock proteins was induced during this host's immunological response, and this information was then used to build a thorough network relating to immunity and the heat-shock response. This is the first study to examine the relationship between pathogenic bacterial infection, disease reversal, and modification of innate and adaptive immunity as well as heat shock response.