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Thêm vào đó, IL-8 được sử dụng lâm sàng như một dấu ấn sinh học của các quá trình viêm. Tuy nhiên, các tác động của IL-8 lên các yếu tố điều chỉnh chính của các đặc tính của bạch cầu neutrophil, chẳng hạn như pH nội bào (pH<sub>i<\u002Fsub>), phụ thuộc vào các protein vận chuyển ion và trong quá trình viêm vẫn chưa được làm sáng tỏ. Do đó, chúng tôi đã điều tra chi tiết những thay đổi cơ bản trong pH<sub>i<\u002Fsub>, hình dạng tế bào và hoạt động hóa học được khơi dậy bởi IL-8. Sử dụng các phương pháp chảy tế bào, chúng tôi xác định rằng hoạt động tế bào được kích thích bởi IL-8 phần lớn phụ thuộc vào các kênh ion và bơm vận chuyển cụ thể, chẳng hạn như exchanger natri-hydro (NHE1) và dòng natri không phụ thuộc NHE1. Việc tiếp xúc neutrophil trong ống nghiệm với môi trường viêm vi mô có chứa N-formyl-Met-Leu-Phe, LPS, hoặc IL-8 đã dẫn đến phản ứng giảm về việc tăng kích thước tế bào và pH. Động lực chi tiết của sự giảm phản ứng của bạch cầu neutrophil có thể được minh họa trong một phép đo cytofluorimetric gần như thời gian thực. Cuối cùng, sự suy giảm do LPS tác động đến phản ứng do IL-8 gây ra ở bạch cầu neutrophil đã được xác nhận trong một mô hình máu toàn phần của con người không sử dụng động vật, có tính chuyển giao. Tổng thể, chúng tôi cung cấp những hiểu biết cơ chế mới về sự tương tác của IL-8 với bạch cầu neutrophil và báo cáo chi tiết về sự thay đổi của nó trong tình trạng viêm hệ thống.\u003C\u002Fjats:p>","\u003Cjats:p>A sufficient response of neutrophil granulocytes stimulated by interleukin (IL)-8 is vital during systemic inflammation, for example, in sepsis or severe trauma. Moreover, IL-8 is clinically used as biomarker of inflammatory processes. However, the effects of IL-8 on cellular key regulators of neutrophil properties such as the intracellular pH (pH<sub>i<\u002Fsub>) in dependence of ion transport proteins and during inflammation remain to be elucidated. Therefore, we investigated in detail the fundamental changes in pH<sub>i<\u002Fsub>, cellular shape, and chemotactic activity elicited by IL-8. Using flow cytometric methods, we determined that the IL-8-induced cellular activity was largely dependent on specific ion channels and transporters, such as the sodium-proton exchanger 1 (NHE1) and non-NHE1-dependent sodium flux. Exposing neutrophils in vitro to a proinflammatory micromilieu with N-formyl-Met-Leu-Phe, LPS, or IL-8 resulted in a diminished response regarding the increase in cellular size and pH. The detailed kinetics of the reduced reactivity of the neutrophil granulocytes could be illustrated in a near-real-time flow cytometric measurement. 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Trong ngữ cảnh này, tự thực bào thực hiện chức năng kiểm soát chất lượng chất nguyên sinh và dinh dưỡng bằng cách loại bỏ các bào quan không còn hoạt động hoặc không được sử dụng, các mục tiêu dạng hạt và vi khuẩn xâm nhập, cũng như qua quá trình tiêu hóa khối lượng chất nguyên sinh. Tuy nhiên, các nghiên cứu gần đây chỉ ra rằng tự thực bào một cách bất ngờ ảnh hưởng đến nhiều con đường tiết ra khác nhau. Tự thực bào tham gia vào việc vận chuyển ra ngoài tế bào một số lượng lớn các protein chất nguyên sinh không đi vào con đường tiết ra thông thường qua bộ máy Golgi mà thay vào đó được tiết ra một cách không chính thống trực tiếp từ chất nguyên sinh. Ở tế bào động vật có vú, một ví dụ điển hình của sự thể hiện này của tự thực bào là sự tiết ra không chính thống của một cytokine pro-inflammatory chính, IL-1β. Bài tổng quan này xem xét khái niệm tự thực bào tiết ra và so sánh, đối chiếu vai trò của tự thực bào trong sự tiết ra của IL-1α và IL-1β. Mặc dù IL-1α và IL-1β có các chức năng viêm bên ngoài liên quan chặt chẽ, nhưng chúng khác nhau về sự kích hoạt trong tế bào, cơ chế tiết ra và cách chúng bị ảnh hưởng bởi tự thực bào. Ví dụ này chỉ ra rằng vai trò của tự thực bào trong tiết ra phức tạp hơn, ít nhất là ở các tế bào động vật có vú, so với quan điểm đơn giản cho rằng các autophagosome cung cấp các phương tiện cho việc tiết ra không chính thống của các protein chất nguyên sinh.\u003C\u002Fjats:p>","\u003Cjats:p>Autophagy (macroautophagy) is often defined as a degradative process and a tributary of the lysosomal pathway. In this context, autophagy carries out cytoplasmic quality control and nutritional functions by removing defunct or disused organelles, particulate targets and invading microbes, and by bulk digestion of the cytoplasm. However, recent studies indicate that autophagy surprisingly affects multiple secretory pathways. 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Các phản ứng miễn dịch bẩm sinh và thích nghi truyền thống thường được coi là riêng biệt, nhưng các bằng chứng mới nổi cho thấy chúng chồng chéo và tương tác lẫn nhau. Các loại tế bào mới được phát hiện, đặc biệt là tế bào lympho bẩm sinh và tế bào ức chế nguồn gốc myeloid, đang thu hút được sự chú ý ngày càng tăng. Ở đây, chúng tôi tóm tắt và làm nổi bật các khái niệm hiện tại trong lĩnh vực này, tập trung vào các tế bào miễn dịch bẩm sinh cũng như bộ máy inflamasome và cảm nhận DNA, những yếu tố có vẻ rất quan trọng cho việc kích hoạt và phối hợp miễn dịch bẩm sinh, và có thể cung cấp những cơ hội điều trị mới cho các bệnh tự miễn, tự viêm và nhiễm trùng.\u003C\u002Fjats:p>","\u003Cjats:p>Innate immunity is a rapidly evolving field with novel cell types and molecular pathways being discovered and paradigms changing continuously. Innate and adaptive immune responses are traditionally viewed as separate from each other, but emerging evidence suggests that they overlap and mutually interact. Recently discovered cell types, particularly innate lymphoid cells and myeloid-derived suppressor cells, are gaining increasing attention. Here, we summarize and highlight current concepts in the field, focusing on innate immune cells as well as the inflammasome and DNA sensing which appear to be critical for the activation and orchestration of innate immunity, and may provide novel therapeutic opportunities for treating autoimmune, autoinflammatory, and infectious diseases.\u003C\u002Fjats:p>",{"EN":1514,"VI":1515},"Cellular Innate Immunity: An Old Game with New Players","Miễn dịch bẩm sinh tế bào: Một trò chơi cũ với những người chơi mới",{"VOID":1517},"28006777",{"VOID":1519},"10.1159\u002F000453397",[146],[148],"https:\u002F\u002Fkarger.com\u002FJIN\u002Farticle\u002Fdoi\u002F10.1159\u002F000453397",[1524,1543,1560,1577,1596,1615],{"id":1525,"sortIndex":25,"researcher":24,"roles":1526,"affiliations":1527,"properties":1536,"displayName":1540,"givenName":24,"familyName":24},"604029fd-6421-4277-b678-9fe622ccdd09",[],[1528],{"id":1529,"sortIndex":25,"affiliation":1530,"properties":24},"0aa8ca2c-e527-495f-867a-8ce095404ead",{"id":1529,"createTime":24,"updateTime":24,"relativeEntities":1531,"slug":24,"properties":1532,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1535,"statistic":24},[],{"title":1533},{"EN":1534},"Institute of Medical Microbiology and Hygiene, University of Freiburg, Freiburg Medical Center, Freiburg,",[],{"orcid":1537,"title":1539,"openalex":1541},{"VOID":1538},"https:\u002F\u002Forcid.org\u002F0000-0001-6986-127X",{"EN":1540},"Georg Gasteiger",{"VOID":1542},"A5011718692",{"id":1544,"sortIndex":98,"researcher":24,"roles":1545,"affiliations":1546,"properties":1555,"displayName":1557,"givenName":24,"familyName":24},"80c0ea38-f19a-4f5e-a0a7-692864eb641f",[],[1547],{"id":1548,"sortIndex":25,"affiliation":1549,"properties":24},"934c857e-fe7d-4b16-81a4-3a7df11690e4",{"id":1548,"createTime":24,"updateTime":24,"relativeEntities":1550,"slug":24,"properties":1551,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1554,"statistic":24},[],{"title":1552},{"EN":1553},"Roche Pharma Research and Early Development (pRED), Immunology, Inflammation and Infectious Diseases (I3) Discovery and Translational Area, Roche Innovation Center Basel, Basel, Switzerland",[],{"title":1556,"openalex":1558},{"EN":1557},"Andrea D’Osualdo",{"VOID":1559},"A5000561086",{"id":1561,"sortIndex":187,"researcher":24,"roles":1562,"affiliations":1563,"properties":1570,"displayName":1574,"givenName":24,"familyName":24},"7fc8b014-504e-48a0-a669-ff63f41c8b57",[],[1564],{"id":1548,"sortIndex":25,"affiliation":1565,"properties":24},{"id":1548,"createTime":24,"updateTime":24,"relativeEntities":1566,"slug":24,"properties":1567,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1569,"statistic":24},[],{"title":1568},{"EN":1553},[],{"orcid":1571,"title":1573,"openalex":1575},{"VOID":1572},"https:\u002F\u002Forcid.org\u002F0000-0002-1190-7623",{"EN":1574},"David Schubert",{"VOID":1576},"A5101896253",{"id":1578,"sortIndex":96,"researcher":24,"roles":1579,"affiliations":1580,"properties":1589,"displayName":1593,"givenName":24,"familyName":24},"b915e872-9f5b-41f9-a368-ec5fd3432fb5",[],[1581],{"id":1582,"sortIndex":25,"affiliation":1583,"properties":24},"6c2b01e9-1cd6-44d5-9419-ec0a61fa41ae",{"id":1582,"createTime":24,"updateTime":24,"relativeEntities":1584,"slug":24,"properties":1585,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1588,"statistic":24},[],{"title":1586},{"EN":1587},"Department of Immunology, Interfaculty Institute for Cell Biology and",[],{"orcid":1590,"title":1592,"openalex":1594},{"VOID":1591},"https:\u002F\u002Forcid.org\u002F0000-0002-8627-7056",{"EN":1593},"Alexander N.R. 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Ở động vật vô xương sống, các protein chứa miền fibrinogen đóng vai trò trong phản ứng phòng vệ chống lại các tác nhân gây bệnh; tuy nhiên, chúng không tham gia vào quá trình đông máu, cho thấy rằng vai trò này mới được hình thành gần đây. Các phân tử chứa mô hình fibrinogen đã được xác định trong nhiều loài động vật vô xương sống khác nhau, và hầu hết các phân tử này đến nay đều liên quan đến phản ứng phòng vệ. Hơn nữa, các dự án giải mã gen gần đây của các động vật vô xương sống đã tiết lộ số lượng gen tương tự như fibrinogen trong bộ gen của chúng, cho thấy các chức năng quan trọng và có thể đa dạng của các protein giống fibrinogen ở động vật vô xương sống. Vai trò tổ tiên của các phân tử chứa miền liên quan đến fibrinogen (FReDs) liên quan đến miễn dịch là trọng tâm của bài đánh giá này, với sự nhấn mạnh vào các FReDs cụ thể được gọi là protein liên quan đến fibrinogen (FREPs) được xác định từ động vật thân mềm truyền bệnh sán máng <i>Biomphalaria glabrata<\u002Fi>. Trong bài viết này, chúng tôi phác thảo phạm vi các loài động vật vô xương sống mà FREPs có thể được tìm thấy, và chi tiết vai trò của những phân tử này trong phòng vệ và bảo vệ chống lại nhiễm trùng.\u003C\u002Fjats:p>","\u003Cjats:p>In vertebrates, the conversion of fibrinogen into fibrin is an essential process that underlies the establishment of the supporting protein framework required for coagulation. In invertebrates, fibrinogen-domain-containing proteins play a role in the defense response generated against pathogens; however, they do not function in coagulation, suggesting that this role has been recently acquired. Molecules containing fibrinogen motifs have been identified in numerous invertebrate organisms, and most of these molecules known to date have been linked to defense. Moreover, recent genome projects of invertebrate animals have revealed surprisingly high numbers of fibrinogen-like loci in their genomes, suggesting important and perhaps diverse functions of fibrinogen-like proteins in invertebrates. The ancestral role of molecules containing fibrinogen-related domains (FReDs) with immunity is the focus of this review, with emphasis on specific FReDs called fibrinogen-related proteins (FREPs) identified from the schistosome-transmitting mollusc <i>Biomphalaria glabrata<\u002Fi>. 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cầu trung tính được tuyển mộ đến vị trí nhiễm trùng hoặc tổn thương, nơi chúng giúp khởi xướng phản ứng viêm cấp tính. Trong những trường hợp viêm vô trùng, khi không có mối đe dọa vi sinh vật, sự tuyển mộ bạch cầu trung tính này được điều hòa bởi việc giải phóng các tín hiệu nguy hiểm hay các mẫu phân tử liên quan đến tổn thương (DAMPs) từ các tế bào và mô bị phá hủy. Trong trạng thái cơ bản, nhiều chất này bị giữ lại và vẫn ẩn giấu bên trong tế bào, nhưng được giải phóng sau khi màng plasma bị vỡ. Trong những trường hợp khác, các DAMP này không được phát hiện bởi hệ thống miễn dịch bẩm sinh trừ khi bị biến đổi hóa học hoặc phân giải proteolytically do tổn thương mô. Các DAMP có thể được bạch cầu trung tính phát hiện trực tiếp và điều chỉnh sự tuyển mộ của chúng đến các vị trí bị tổn thương, hoặc ngược lại, chúng có thể tác động lên các loại tế bào khác, từ đó tạo điều kiện cho sự xuất hiện của bạch cầu trung tính tại vị trí tổn thương. Trong bài tổng quan này, chúng tôi phác thảo các tác động trực tiếp và gián tiếp của một số DAMP, đặc biệt là ATP ngoại bào, các peptide formyl hóa của ty thể và DNA ty thể, tất cả đều được giải phóng từ các tế bào hoại tử. Chúng tôi xem xét ảnh hưởng của các chất này đối với sự tuyển mộ và hành vi của bạch cầu trung tính đến các vị trí tổn thương vô trùng. Chúng tôi cũng làm nổi bật nghiên cứu cho thấy rằng bạch cầu trung tính tham gia tích cực vào việc kích hoạt giai đoạn hồi phục của phản ứng viêm. Bài tổng quan này làm sáng tỏ một cơ sở nghiên cứu ngày càng lớn cho thấy rằng việc giải phóng DAMP và sự influx của bạch cầu trung tính đóng vai trò chức năng quan trọng trong phản ứng viêm, ngay cả khi không có tác nhân gây bệnh nào có mặt.\u003C\u002Fjats:p>","\u003Cjats:p>Neutrophils are recruited to a site of infection or injury where they help initiate the acute inflammatory response. In instances of sterile inflammation, where no microbial threats are present, this neutrophil recruitment is mediated by the release of danger signals or damage-associated molecular patterns (DAMPs) from disrupted cells and tissues. At basal state, many of these substances are sequestered and remain hidden within the cell, but are released following the rupture of the plasma membrane. In other instances, these DAMPs are undetected by the innate immune system unless chemically or proteolytically modified by tissue damage. DAMPs may be directly detected by neutrophils themselves and modulate their recruitment to sites of damage or, alternatively, they can act on other cell types which in turn facilitate the arrival of neutrophils to a site of injury. In this review, we outline the direct and indirect effects of a number of DAMPs, notably extracellular ATP, mitochondrial formylated peptides and mitochondrial DNA, all of which are released by necrotic cells. We examine the effect of these substances on the recruitment and behaviour of neutrophils to sites of sterile injury. We also highlight research which suggests that neutrophils are actively involved in triggering the resolution phase of an inflammatory response. This review brings to light a growing body of work that demonstrates that the release of DAMPs and the ensuing influx of neutrophils plays an important functional role in the inflammatory response, even when no pathogens are present.\u003C\u002Fjats:p>",{"EN":2452,"VI":2453},"Damage-Associated Molecular Patterns Control Neutrophil Recruitment","Các Mẫu Phân Tử Liên Quan Đến Tổn Thương Kiểm Soát Sự Thu hút Bạch Cầu Trung 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tế bào bạch cầu trung tính sử dụng các cơ chế tinh vi để bắt giữ và tiêu diệt các vi sinh vật xâm nhập. Một cơ chế liên quan đến việc giải phóng chromatin đã được giải nén ra khỏi tế bào. Các vi sinh vật được giữ lại bởi chromatin ngoại bào và tiếp xúc với nồng độ cao của các hợp chất diệt khuẩn. Chúng tôi đã xem xét quy định của việc giải phóng chromatin bằng cách kiểm tra sự đóng góp của vi ống và bộ khung tế bào actin đối với việc triển khai các bẫy ngoại bào của bạch cầu trung tính (NETs). Việc nuôi cấy tế bào bạch cầu trung tính của người với nocodazole, một chất ức chế polymer hóa tubulin, hoặc cytochalasin D, một chất ức chế sự hình thành vi sợi actin, đã làm giảm nghiêm trọng khả năng của bạch cầu trung tính trong việc đáp ứng với LPS bằng cách giải phóng chromatin khỏi các tế bào. Ngoài ra, việc tiền xử lý bạch cầu trung tính với M1\u002F70, một kháng thể đơn dòng đối với thụ thể kết dính Mac-1 integrin, đã giảm mạnh việc triển khai chromatin vào NETs. Phân tích sự deimination histone, quá trình chuyển đổi arginine thành citrulline trong 3 trong 4 histone lõi bởi peptidylarginine deiminase 4, cho thấy rằng các liệu pháp ức chế sự hình thành NET cũng làm giảm sự deimination histone. Dữ liệu của chúng tôi chỉ ra rằng việc hình thành NET yêu cầu vi tubulin và vi sợi actin hoạt động và phản ứng với sự tham gia của các integrin Mac-1. Bởi vì sự deimination histone xảy ra đồng thời với việc giải phóng NET, chúng tôi đề xuất rằng những sự kiện này đại diện cho các cơ chế chồng chéo trong phản ứng của bạch cầu trung tính đối với các nhiễm trùng.\u003C\u002Fjats:p>","\u003Cjats:p>Neutrophils use intricate mechanisms for capturing and killing invading microorganisms. One mechanism entails the release of relaxed chromatin from the cell. Microbes are trapped by the extracellular chromatin and exposed to high local concentrations of bactericidal compounds. We examine the regulation of chromatin release by testing the contribution of microtubules and the actin cytoskeleton to the deployment of neutrophil extracellular traps (NETs). Incubation of human neutrophils with nocodazole, a tubulin polymerization inhibitor, or cytochalasin D, an inhibitor of actin filamentation, severely diminished the ability of neutrophils to respond to LPS by releasing chromatin from the cells. In addition, pretreatment of neutrophils with M1\u002F70, a monoclonal antibody to the Mac-1 integrin adhesion receptor, drastically reduced the deployment of chromatin into NETs. Analysis of histone deimination, the conversion of arginine to citrulline in 3 of the 4 core histones by peptidylarginine deiminase 4, revealed that the treatments inhibiting NET formation also reduced histone deimination. Our data indicate that NET formation requires functional tubulin and actin filaments and responds to engagement of Mac-1 integrins. 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Các protein tự thực bào đơn lẻ hoặc các bộ thiết bị cốt lõi của cơ chế tự thực bào cũng có thể hoạt động như các yếu tố kháng virus độc lập với đường dẫn tự thực bào kinh điển. Hơn nữa, để tồn tại và phát triển trong cơ thể chủ, virus đã phát triển nhiều chiến lược khác nhau để tránh khỏi cuộc tấn công của quá trình tự thực bào và thao túng cơ chế tự thực bào để phục vụ cho lợi ích của chúng. Bài tổng quan này tóm tắt những bước tiến gần đây trong việc hiểu rõ vai trò kháng virus và hỗ trợ virus của tự thực bào cũng như các chức năng độc lập với tự thực bào của các gen liên quan đến tự thực bào mà trước đây chưa được đánh giá cao.","\u003Cjats:p>The autophagy pathway is an essential component of host defense against viral infection, orchestrating pathogen degradation (xenophagy), innate immune signaling, and certain aspects of adaptive immunity. 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