幽門桿菌感染人體胃部後，菌體利用本身附著因子SabA和sialyl Lewis x作用而貼附並群居於發炎的胃黏膜表面，導致持續性感染，本實驗室早先的研究中發現，台灣的臨床菌株中，有三分之二的菌株其sabA的ORF內含有一段CT雙核苷重複序列，這類菌株定義為第一型，其sabA的蛋白表現會受到CT雙核苷重複序列數目的影響。第二型的菌株，則在ORF內不帶有CT雙核苷重複序列，故sabA的表現並不受到CT雙核苷重複序列的影響。而CT雙核苷重複序列的數目會受到slipped strand mispairing (SSM) 的機制影響¬而改變，因此，sabA的表現在轉譯的層次上可被SSM所調控。
本研究的第一部分主要探討在轉譯層次上對sabA的調控，Hp323以及Hp779進行CT雙核苷重複序列數目分析後，定義為不表現SabA蛋白的菌株，然而西方墨點法的結果卻呈現SabA陽性反應。因此本研究以sequencing gel及lacZ報導系統對SSM的機制進行分析，發現這種SSM的機制會導致同ㄧ個細菌族群中產生帶有不同CT雙核苷重序列數目的細菌。另外，mismatch也會導致某些sabA phase on菌株提早出現轉譯終止密碼而無法轉譯出完整蛋白。
本研究中第二個部分主要進行胃幽門桿菌sabA基因轉錄之分析，發現sabA基因的表現主要在對數生長期，經由5’RACE結果發現在J99標準菌株中，sabA轉錄起始點為轉譯起始密碼上游66個鹼基對的位置，而在臨床菌株Hp258，轉錄起始點則為轉譯起始密碼上游64個鹼基對的位置。經由115株臨床菌株定序的分析結果，sabA基因啟動子附近區域之DNA序列在不同菌株之間則有一段具變異的polyT重複序列。此外，sabA在不同菌株間轉錄的活性差異很大，而這些差異也和polyT的數目呈現統計相關性，經統計分析的結果發現，polyT的數目與SabA蛋白表現情形、胃幽門桿菌菌落量以及急性發炎指數呈現統計相關性，而這段polyT的數目也可以藉由SSM加以調控。此外，高變異度的sabA啟動子區域序列可能影響轉錄因子的結合而影響轉錄活性。
本研究的第三個部分在探討是否有其他環境因子可影響sabA的表現，本研究發現酸性的培養環境不會顯著影響sabA在菌株Hp258的表現，然而將Hp258培養在Brucella培養液中，並加入經Hp238感染MKN45細胞株後的上清液，我們發現sabA在Hp258的表現量有顯著增加的趨勢。
綜合以上的結果，sabA的表現以及調控為相當複雜的機制，包含(1)在轉譯層次上藉由改變CT雙核苷重複序列的數目¬而調控SabA蛋白的表現，(2)在感染過程中，細胞株或細菌本身也會釋出某些因子而刺激sabA的表現，(3)sabA的表現可以在轉錄的層次上受到調控，高變異度的啟動子區域可以藉由影響轉錄因子結合，或者藉
SSM改變polyT序列的數目，進而影響sabA在轉錄上的活性。

Helicobacter pylori exploit sialyl acid binding adhesin (SabA) to interact with sialyl Lewis x to establish persistent colonization on inflamed gastric mucosal surface. In our previous study, two third of sabA strains in Taiwan are the first type (Type I) which have different CT repeats to make sabA in frame or out of frame, and there is a specific deletion type (Type II) of sabA-positive strains in their CT repeat region. The CT repeat number can change due to slipped strand mispairing (SSM). Therefore, the expression of sabA can be regulated by SSM at the translational level.
The first part of this study was to understand the regulatory mechanism of sabA at translational level. We found Hp323 and Hp779 were SabA negative strains predicted by CT repeats, but the western blotting result showed SabA was detectable in both strains. The result of sequencing gel and lacZ reporter system showed that SSM created a mixture of CT repeats in the population. The mismatch introduced an early stop codon in some phase on strains and truncated protein was expressed in these strains.
The second part of this study was to analyze the transcriptional pattern of sabA in H. pylori. The expression of sabA was more in log phase. The results of 5’ RACE revealed that the transcriptional start point of sabA was 66 bp upstream of ATG in reference strain J99 and 64 bp upstream in Hp258. The sequence results of 115 clinical strains revealed that there was a variable polyT tract closed to the promoter region of sabA. The transcriptional activity of sabA was dramatically different in clinical strains, and this result was correlated to the numbers of polyT tract. The statistic results showed polyT tract was correlated with the expression of SabA, H. pylori density and acute inflammatory score (AIS). The results also showed that the polyT tract was also regulated by SSM to create varying lengths of polyT tract in a population. Highly variable promoter region of sabA in H. pylori also affect the transcription of sabA by affecting binding of transcription factors.
The third part of this study was to investigate whether other factors affect the expression of sabA. We found the expression of sabA in Hp258 cultured in low pH was not dramatically decreased than in natural pH. On the other hand, the expression of sabA was increased in Hp258 cultured in brucella broth containing 10% horse serum and supernatant collected from the MKN45 cells infected with Hp238.
In conclusion, the expression and regulation of sabA is complicated, including the regulation of CT repeats by SSM at the translational level and variation of CT repeats leading to the full length or truncated protein. In the process of infection, the factors released from host cells or H. pylori stimulate the expression of sabA. On the other hand, the promoter region is highly variable between clinical strains. Such variation of sequence affects the binding of transcriptional factor and the variation of
polyT tract closed to promoter region dramatically affects the transcription of sabA.

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