15.4
病原体の植民
宿主組織への病原体定着は、感染症の発症において重要なステップです。細菌、菌類、ウイルス、原生動物など様々な病原性微生物は、宿主環境に付着し、侵入し、存続するための複雑な戦略を進化させてきました。これらのメカニズムにより、病原体は感染を確立し、免疫応答を回避し、抗菌薬治療に抵抗します。
宿主細胞への付着
…
多くの原核生物および真核生物の病原体は、すぐに病気を引き起こすことなく宿主組織に定着できます。感染は、定着によって組織損傷や宿主の炎症反応が生じた場合のみ発生します。
細菌は宿主細胞に付着することでコロナレーションを開始します。
一部の細菌は、呼吸器などの上皮細胞に固定する毛皮(ピリ)や軟骨毛(フィムブリア)を持っています。
多くの病原性細菌は表面タンパク質である癒着性を発現し、宿主細胞への付着を強化するのに役立ちます。
付着後、病原体は宿主に定着し始めます。
特定の細菌はバイオフィルムを形成し、免疫攻撃や治療抵抗からの保護を提供します。
定着後、特定の病原体はヒアルロニダーゼやコアグラーゼなどの酵素を産生し、感染中の組織侵入を促進します。
特定の病原体はカプセルを形成し、抗原構造を覆い隠し、免疫細胞による食細胞作用を防いでいます。
あるいは、抗原変異によって特定の病原体が表面タンパク質を改変して免疫を回避し、定着を拡大することが可能になります。
View the full transcript and gain access to JoVE Core videos
Q1: How do bacteria initially attach to host cells during colonization?
Bacteria initiate colonization by using specialized structures like pili or fimbriae to anchor to epithelial cells in areas such as the respiratory tract. Many pathogenic bacteria also express surface proteins called adhesins, which strengthen attachment by recognizing and binding to extracellular matrix components or cell surface molecules on host cells.
Q2: What is the difference between colonization and infection?
Colonization occurs when pathogens attach to and establish themselves within host tissues without immediately causing disease. Infection develops only when colonization leads to tissue damage or triggers a host inflammatory response. Many prokaryotic and eukaryotic pathogens can colonize tissues for extended periods before progressing to active infection.
Q3: How do biofilms protect bacteria from immune attacks?
Biofilms are structured communities of bacteria encased in a self-produced extracellular matrix that provides enhanced protection against phagocytosis and antimicrobial agents. This protective structure significantly increases pathogen persistence within the host. Quorum sensing, a form of bacterial communication via signaling molecules, regulates biofilm formation and virulence factor expression.
Q4: What enzymes do pathogens produce to facilitate tissue invasion?
Pathogens produce enzymes such as hyaluronidase and coagulase to facilitate tissue invasion. Hyaluronidase breaks down hyaluronic acid in connective tissues, aiding tissue penetration, while coagulase induces fibrin clot formation that may shield bacteria from immune cells. These enzymatic secretions help pathogens establish deeper infections within host tissues.
Q5: How do bacterial capsules help pathogens evade the immune system?
Bacterial capsules are composed of polysaccharides that mask antigenic cell surface components, preventing recognition and phagocytosis by immune cells. This immune evasion strategy allows pathogens to avoid detection and elimination. Capsules represent one of several mechanisms pathogens use to establish persistent infections and resist host defenses.
Q6: What is antigenic variation and how does it extend colonization?
Antigenic variation is a mechanism in which pathogens alter surface protein structures to escape recognition by host antibodies. This strategy allows prolonged colonization and chronic or relapsing infections. Pathogens such as Neisseria gonorrhoeae and Trypanosoma brucei are well known for using antigenic variation to evade immune detection and maintain persistent infections.
Q7: How do intracellular pathogens like Listeria monocytogenes avoid immune surveillance?
Some bacteria adopt an intracellular lifestyle to circumvent immune surveillance by invading host cells and exploiting the host cytoskeleton. These pathogens use actin-based motility structures, commonly termed actin rockets, to propel themselves and enable direct cell-to-cell transmission. This intracellular movement minimizes exposure to extracellular immune defenses and represents a key determinant of bacterial pathogenicity and virulence.