{"id":11408,"date":"2026-01-14T12:34:00","date_gmt":"2026-01-14T08:34:00","guid":{"rendered":"https:\/\/medscriptum.org\/?p=11408"},"modified":"2026-01-14T12:34:56","modified_gmt":"2026-01-14T08:34:56","slug":"new-aspects-of-tuberculosis-pathogenesis","status":"publish","type":"post","link":"https:\/\/medscriptum.org\/en\/new-aspects-of-tuberculosis-pathogenesis\/","title":{"rendered":"New Aspects of Tuberculosis Pathogenesis"},"content":{"rendered":"<p style=\"text-align: justify\" data-path-to-node=\"3\">The biological resilience of the tuberculosis causative agent (<i data-path-to-node=\"3\" data-index-in-node=\"63\">Mycobacterium tuberculosis<\/i>) lies in its unique adaptive ability. The bacterium alters the body&#8217;s immune response to its own advantage and uses it for survival. <a href=\"https:\/\/news.exeter.ac.uk\/mrc-centre-for-medical-mycology\/tb-harnesses-part-of-immune-defence-system-to-cause-infection\/\" target=\"_blank\" rel=\"noopener\">A research team<\/a> has made this process even clearer. It was discovered that the bacterium modifies the function of the Dectin-1 receptor, and as a result, instead of destroying the pathogen, the receptor facilitates its survival. Through this mechanism, the tuberculosis pathogen inhibits cellular self-cleansing and multiplies unhindered within macrophages.<\/p>\n<p style=\"text-align: justify\" data-path-to-node=\"4\">The study showed that the bacterium uses a specific carbohydrate, Alpha-glucan, to purposefully bind to the Dectin-1 receptor. Under normal conditions, this contact should result in the destruction of the pathogen; however, in the case of tuberculosis, the process develops quite differently: the mTOR protein is activated, which halts the process of autophagy inside the cell.<\/p>\n<p style=\"text-align: justify\" data-path-to-node=\"5\">In this way, the bacterium avoids lysosomal degradation and creates a favorable environment for survival within macrophages. Experimental models confirmed that when the Dectin-1 receptor is blocked, the bacterial load is reduced tenfold. These data once again confirm the decisive role of this receptor in the development of the infection.<\/p>\n<p style=\"text-align: justify\" data-path-to-node=\"6\"><strong>The Role of Alpha-glucan<\/strong><\/p>\n<p style=\"text-align: justify\" data-path-to-node=\"7\">Structural analysis showed that the core of this mechanism is the bacterial branched Alpha-glucan. This finding was unexpected because the Dectin-1 receptor was previously considered a response mechanism only for fungal infections. The research revealed that the tuberculosis pathogen has evolutionarily acquired the ability to bind with this receptor to alter the host cell&#8217;s immune signaling.<\/p>\n<p style=\"text-align: justify\" data-path-to-node=\"8\">These data lay the foundation for a completely new method of treatment: &#8220;Host-directed therapy.&#8221; Its essence lies in the fact that instead of acting directly on the pathogen &#8211; which is often resistant to antibiotics &#8211; we can restore the altered immune signaling of the host cell.<\/p>\n<p style=\"text-align: justify\">Source: <a href=\"https:\/\/www.science.org\/doi\/10.1126\/sciimmunol.adw0732\" target=\"_blank\" rel=\"noopener\">Science Immunology<\/a><\/p>\n<p style=\"text-align: justify\"><br style=\"font-weight: 400\" \/><br style=\"font-weight: 400\" \/><\/p>\n","protected":false},"excerpt":{"rendered":"<p>The biological resilience of the tuberculosis causative agent (Mycobacterium tuberculosis) lies in its unique adaptive ability. The bacterium alters the body&#8217;s immune response to its own advantage and uses it for survival. A research team has made this process even clearer. It was discovered that the bacterium modifies the function of the Dectin-1 receptor, and [&hellip;]<\/p>\n","protected":false},"author":5,"featured_media":11409,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"_acf_changed":false,"footnotes":""},"categories":[1587],"tags":[3829,3734,2094],"class_list":["post-11408","post","type-post","status-publish","format-standard","has-post-thumbnail","category-research","tag-pathogenesis","tag-resistance","tag-tuberculosis"],"acf":[],"_links":{"self":[{"href":"https:\/\/medscriptum.org\/en\/wp-json\/wp\/v2\/posts\/11408","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/medscriptum.org\/en\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/medscriptum.org\/en\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/medscriptum.org\/en\/wp-json\/wp\/v2\/users\/5"}],"replies":[{"embeddable":true,"href":"https:\/\/medscriptum.org\/en\/wp-json\/wp\/v2\/comments?post=11408"}],"version-history":[{"count":2,"href":"https:\/\/medscriptum.org\/en\/wp-json\/wp\/v2\/posts\/11408\/revisions"}],"predecessor-version":[{"id":11414,"href":"https:\/\/medscriptum.org\/en\/wp-json\/wp\/v2\/posts\/11408\/revisions\/11414"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/medscriptum.org\/en\/wp-json\/wp\/v2\/media\/11409"}],"wp:attachment":[{"href":"https:\/\/medscriptum.org\/en\/wp-json\/wp\/v2\/media?parent=11408"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/medscriptum.org\/en\/wp-json\/wp\/v2\/categories?post=11408"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/medscriptum.org\/en\/wp-json\/wp\/v2\/tags?post=11408"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}