Vibrio cholerae, the causative agent of cholera, is commonly isolated, along with other bacterial species, from chironomid insects (Diptera: Chironomidae). Nevertheless, its prevalence in the chironomid egg masses’ microbiota is less than 0.5%. V. cholerae secretes haemagglutinin/protease (HAP) that degrades the gelatinous matrix of chironomid egg masses and prevents hatching. Quorum sensing (QS) activates HAP production in response to accumulation of bacterial autoinducers (AIs). Our aim was to define the impact of chironomid microbiota on HAP production by V. cholerae. To study QS signaling, we used V. cholerae bioluminescence reporter strains (QS‐proficient O1 El‐Tor wild‐type and QS‐deficient mutants) and different bacterial species that we isolated from chironomid egg masses. These egg mass isolates, as well as a synthetic AI‐2, caused an enhancement in lux expression by a V. cholerae QS‐deficient mutant. The addition of the egg mass bacterial isolate supernatant to the QS‐deficient mutant also enhanced HAP production and egg mass degradation activities. Moreover, the V. cholerae wild‐type strain was able to proliferate using egg masses as their sole carbon source, while the QS‐deficient was not. The results demonstrate that members of the chironomid bacterial consortium produce external chemical cues that, like AI‐2, induce expression of the hapA gene in V. cholerae. Understanding the interactions between V. cholerae and the insects’ microbiota may help uncover the interactions between this pathogen and the human gut microbiota.

中文翻译：

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蛋壳微生物群的群体感应信号影响霍乱弧菌的血凝素/蛋白酶（HAP）产生

霍乱弧菌是霍乱的病原体，通常与其他细菌一起从尺虫中分离出来（双翅目：:科）。然而，其在鸡卵虫的微生物群中的患病率小于0.5％。霍乱弧菌分泌血凝素/蛋白酶（HAP），可降解Chironomid卵团的胶状基质并防止孵化。群体感应（QS）响应细菌自身诱导物（AI）的积累激活HAP的产生。我们的目的是确定拟杆菌对霍乱弧菌产生HAP的影响。为了研究QS信号传导，我们使用了霍乱弧菌生物发光报告菌株（QS精制的O1 El-Tor野生型和QS精制的突变体）和我们从蛋壳虫卵中分离出的不同细菌种类。这些鸡蛋分离物以及人工合成的AI-2导致霍乱弧菌QS缺陷型突变体的lux表达增强。向QS缺陷型突变体中添加卵团细菌分离物上清液也可提高HAP产量和卵团降解活性。此外，霍乱弧菌野生型菌株能够利用卵团作为唯一碳源进行增殖，而QS缺乏则不能。结果表明，手性细菌联盟的成员产生了外部化学线索，像AI-2一样，诱导了hapA的表达。霍乱弧菌中的基因。了解霍乱弧菌与昆虫微生物群之间的相互作用可能有助于揭示该病原体与人类肠道微生物群之间的相互作用。