<?xml-model href='http://www.tei-c.org/release/xml/tei/custom/schema/relaxng/tei_all.rng' schematypens='http://relaxng.org/ns/structure/1.0'?><TEI xmlns="http://www.tei-c.org/ns/1.0">
	<teiHeader>
		<fileDesc>
			<titleStmt><title level='a'>Gut bacteria induce heterologous immune priming in Rhodnius prolixus encompassing both humoral and cellular immune responses</title></titleStmt>
			<publicationStmt>
				<publisher>Public Library of Science</publisher>
				<date>12/01/2025</date>
			</publicationStmt>
			<sourceDesc>
				<bibl> 
					<idno type="par_id">10660069</idno>
					<idno type="doi">10.1371/journal.ppat.1012947</idno>
					<title level='j'>PLOS Pathogens</title>
<idno>1553-7374</idno>
<biblScope unit="volume">21</biblScope>
<biblScope unit="issue">12</biblScope>					

					<author>Carissa A Gilliland</author><author>Loretta Mugo-Kamiri</author><author>Sara Martin</author><author>Kevin J Vogel</author><author>Pedro F Vale</author>
				</bibl>
			</sourceDesc>
		</fileDesc>
		<profileDesc>
			<abstract><ab><![CDATA[<p>Insects lack the adaptive, antibody mediated responses of vertebrates, yet they possess a robust innate immune system capable of defending themselves against pathogens. Immune priming has been observed in multiple insect species, wherein exposure to a pathogen provides protection against subsequent infections by the pathogen. Heterologous immune priming has also been described, where presence of one bacterial species provides protection against another. We determined that<italic>Rhodococcus rhodnii</italic>, a gut symbiont of the kissing bug<italic>Rhodnius prolixus,</italic>induces strong heterologous immune priming, while axenic bugs lacking gut bacteria are highly susceptible to pathogens. Commensal<italic>Escherichia coli</italic>provides less robust protection.<italic>R. rhodnii</italic>must be alive within the insect as dead bacteria do not stimulate immune priming and pathogen resistance. Removal of<italic>R. rhodnii</italic>from the gut reduces resistance to pathogens while restoring it to axenic bugs improves pathogen resistance, though not completely. Unlike most other examples of symbiont-mediated immune priming, we find no evidence that<italic>R. rhodnii</italic>ever leaves the gut, despite activating a potent immune response in the hemocoel and fat body.<italic>R. rhodnii</italic>and<italic>E. coli</italic>activate both the IMD and Toll pathways indicating cross-activation of the pathways, while silencing of either pathway leads to a loss of the protective effect. Several antimicrobial peptides are induced in the fat body by presence of gut bacteria. When<italic>E. coli</italic>is in the gut, expression of antimicrobial peptides is often higher than when<italic>R. rhodnii</italic>is present, while<italic>R. rhodnii</italic>induces proliferation of hemocytes and induces a stronger melanization response than<italic>E. coli</italic>. Hemolymph from<italic>R. rhodnii</italic>bugs has a greater ability to convert the melanin precursor DOPA to melanization products than axenic or<italic>E. coli</italic>-harboring bugs. These results demonstrate that<italic>R. rhodnii’s</italic>benefits to its host extend beyond nutritional provisioning, playing an important role in the host immune system.</p>]]></ab></abstract>
		</profileDesc>
	</teiHeader>
	<text><body><div/></body></text>
</TEI>
