Host-to-Host Group A Streptococcus Transmission Causes Infection of the Lamina Propria but Not Epithelium of the Upper Respiratory Tract in MyD88-Deficient Mice.
Host-to-Host Group A Streptococcus Transmission Causes Infection of the Lamina Propria but Not Epithelium of the Upper Respiratory Tract in MyD88-Deficient Mice.
复制标题
在 MyD88 缺陷小鼠中，宿主间 A 组链球菌传播会导致固有层感染，但不会导致上呼吸道上皮感染。
DOI：
10.1128/iai.00423-21
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发表时间：
2022
影响因子：
3.1
通讯作者：
Lei,Benfang
中科院分区：
文献类型：
--
作者：
Minor,Dylan;Cavon,Jacob;Johnson,Thea;Ontiveros,Savannah;Gao,Daniel;Quinn,MarkT;Lei,Benfang
为了了解针对A组链球菌呼吸道感染发作的保护性免疫应答，我们研究了MyD 88 KO小鼠是否对通过传播的急性感染易感。与鼻内接种A组链球菌（GAS）的小鼠混合后，MyD 88 −/−受体小鼠鼻腔和咽喉中的GAS负荷增加，第7天达到平均咽喉定植6.3 × 106 CFU/拭子和平均鼻腔GAS负荷5.2 × 108 CFU。超过第7天，MyD 88 −/−受体小鼠变得濒死，咽喉和鼻腔中的平均GAS分别为1.6 × 107 CFU/拭子和2.5 × 109 CFU。全身性GAS感染发生在上呼吸道感染后几天。GAS感染唇部、切牙的龈沟和鼻甲的固有层，但不感染鼻腔和鼻咽道上皮，并且C57 BL/6 J受体小鼠的鼻腔和咽喉中没有或低水平的GAS。MyD 88 −/−小鼠的直接鼻腔GAS接种引起GAS感染，主要在鼻甲的固有层中。相比之下，接种GAS的C57 BL/6 J小鼠在鼻腔中有GAS细菌，但在鼻甲的固有层中没有。因此，MyD 88 −/−小鼠通过传播对急性和致命的GAS感染高度敏感，MyD 88信号传导对于保护呼吸道固有层而不是鼻和鼻咽上皮免受GAS感染至关重要。
To understand protective immune responses against the onset of group A Streptococcus respiratory infection, we investigated whether MyD88 KO mice were susceptible to acute infection through transmission. After commingling with mice that had intranasal group A Streptococcus (GAS) inoculation, MyD88−/−recipient mice had increased GAS loads in the nasal cavity and throat that reached a mean throat colonization of 6.3 × 106CFU/swab and mean GAS load of 5.2 × 108CFU in the nasal cavity on day 7. Beyond day 7, MyD88−/−recipient mice became moribund, with mean 1.6 × 107CFU/swab and 2.5 × 109CFU GAS in the throat and nasal cavity, respectively. Systemic GAS infection occurred a couple of days after the upper respiratory infection. GAS infects the lip, the gingival sulcus of the incisor teeth, and the lamina propria of the turbinate but not the nasal cavity and nasopharyngeal tract epithelia, and C57BL/6J recipient mice had no or low levels of GAS in the nasal cavity and throat. Direct nasal GAS inoculation of MyD88−/−mice caused GAS infection, mainly in the lamina propria of the turbinate. In contrast, C57BL/6J mice with GAS inoculation had GAS bacteria in the nasal cavity but not in the lamina propria of the turbinates. Thus, MyD88−/−mice are highly susceptible to acute and lethal GAS infection through transmission, and MyD88 signaling is critical for protection of the respiratory tract lamina propria but not nasal and nasopharyngeal epithelia against GAS infection.