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NEYTROFILLARNING DASTLABKI FAOLLASHUVI HAMDA PHNING KICHIK SILJISHLARI QANDAY QILIB KATTA YALLIG'LANISH JARAYONINI YUZAGA KELTIRADI

Authors: Saydalixo'jaeva Sayyora Zamanovna; Jabborov Botir Baxodir o`g`li; Xalilov Hikmatulla Dilshodovich;

NEYTROFILLARNING DASTLABKI FAOLLASHUVI HAMDA PHNING KICHIK SILJISHLARI QANDAY QILIB KATTA YALLIG'LANISH JARAYONINI YUZAGA KELTIRADI

Abstract

Neytrofillar – organizmning tug‘ma immun tizimining birinchi javob beruvchi hujayralari bo‘lib, ularning yallig‘lanish o‘chog‘iga to‘planishi va faollashuvi murakkab bosqichlardan iborat jarayondir. So‘nggi o‘n yillikdagi tadqiqotlar neytrofillarning to‘liq faollashuvidan oldingi "priming" (tayyorgarlik) bosqichi mavjudligini aniqladi. Bu bosqichda hujayralar mikromuhitdagi kuchsiz signallarga, xususan, pH (vodorod ko‘rsatkichi) o‘zgarishiga nihoyatda sezgir bo‘ladi . An’anaviy qarashda pH neytralligi (7,35-7,45) gomeostazning asosi hisoblansa-da, so‘nggi yillarda yallig‘lanish, ishemiya va o‘sma mikromuhitida yuz beradigan hatto 0,3-0,5 birliklik kichik asidifikatsiya (kislotalashish) neytrofillarning funktsional holatini tubdan o‘zgartirishi mumkinligi isbotlandi . Ushbu maqola neytrofil “priming”i jarayonida ekstratsellyular (hujayradan tashqari) va intrasellyular (hujayra ichi) pH ning roli haqidagi 2015-2025 yillardagi ilg‘or tadqiqotlarni tahlil qiladi. Xususan, pH ning neytrofillar yuzasidagi kimyoatraktant retseptorlari (C5aR, FPR1) ekspressiyasiga, hujayra ichi signal yo‘llariga (fosfoinozitid-3-kinaza - PI3K, mitogen-aktivatsiyalangan protein kinaza - MAPK, Cdc42 GTPazasi) va yadroviy faktor kappa B (NF-κB) faolligiga ta’siri muhokama qilinadi . Shuningdek, suyak ko‘migidagi neytropoez (neytrofillar ishlab chiqarilishi) jarayonining surunkali yallig‘lanish va kislotali muhit tomonidan qayta dasturlanishi va bu holat tizimli yallig‘lanish kasalliklari (artrit, ateroskleroz) bilan bog‘liqligi yoritiladi . Tadqiqotlar shuni ko‘rsatadiki, pH ning kichik siljishi neytrofillarda leykotrien B4 (LTB4) ishlab chiqarilishini kuchaytiradi, NF-κB/STAT3 signal yo‘li orqali ularning yashash muddatini uzaytiradi va neytrofil hujayra tashqi tuzoqlari (NETosis) jarayonini faollashtiradi . Natijada, bu "priming" dan o‘tgan neytrofillar keyingi kuchli stimullarga (masalan, bakterial peptidlar) nisbatan haddan tashqari kuchli javob berib, to‘qimalarning shikastlanishiga va yallig‘lanishning surunkali tus olishiga sabab bo‘ladi. Maqolada, shuningdek, neytrofil faolligini va yallig‘lanishni nazorat qilishda pH sezgir nano-dori tizimlari va NHE1 (Natriy-vodorod almashinuvchisi 1) ingibitorlarining terapevtik potensiali haqidagi so‘nggi yutuqlar ham ko‘rib chiqiladi .

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selected citations
These citations are derived from selected sources.
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
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Average
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