幽門桿菌屬於微需氧、帶有鞭毛的螺旋狀革蘭氏陰性桿菌，也是造
成胃炎、胃潰瘍、十二指腸潰瘍、胃癌甚至胃黏膜淋巴癌的主要病源菌。
利用帶鞘的單端鞭毛產生的運動性被認為是造成幽門桿菌群居的主要因
素。然而鞭毛結構基因所扮演的角色除了f laA 、flaB 、fliD 及flgE 外尚
不清楚。為了解flgK 基因(Hook-Associated Protein 1)在鞭毛形成過程及
功能上的影響，先針對97 株隨機取樣之臨床分離株，利用聚合?連鎖反
應測定均帶有flgK 基因後，由其中任意挑選一株病人為十二指腸潰瘍的
菌株HP250 ，由其選殖flgK 基因，並進行基因序列分析，發現整段基因
由1,821 bp 所組成，和已發表的幽門桿菌26695 及J99 分別有95.7 ﹪及
94.8 ﹪的相似度；在蛋白質組成，預估含606 個氨基酸，也與其分別有
97.9 ﹪及98.0 ﹪的相似度。利用氯黴素抗藥基因片匣插入flgK 染色體基
因，再以基因置換方式產生基因突變株SW805 。突變株以南方墨漬及西
方墨漬試驗證實其正確性後，於電子顯微鏡觀察，可發現野生株具有單
端鞭毛，且其末端具有球棒狀的鞘，在半固體培養基中也具有往外游走
的能力；而突變株不但不具鞭毛亦無游走現象。雖然體外AGS 細胞的附
著能力在測試上野生株與突變株並無顯著差異，但是在BALB/c 的動物
試驗中卻發現，野生株和突變株均能在BALB/c 小鼠的胃內附著，而細
菌附著量野生株明顯地比突變株多，且感染程度也比突變株嚴重。這些
結果顯示flgK 基因在幽門桿菌鞭毛形成的過程中屬於必要的成份，也是
影響幽門桿菌在老鼠胃粘膜群居的重要因素之一。

Helicobacter pylori is a gram-negative, microaerophilic, spiral-shaped
and flagellated microorganism that has been associated with active chronic
gastritis, peptic ulcers and an early risk factor for gastric cancer. Flagellar is
recognized as a major factor in the colonizing ability of H. pylori. However,
the functional roles of flagellar structure genes other than flaA, flaB, fliD and
flgE are not well understood. In an effort to elucidate the function of the flgK
gene, which encodes hook-associated protein 1, in flagellar morphogenesis
and motility, the flgK gene was detected in all of 97 clinical isolates by PCR.
The flgK gene was then cloned from a duodenal ulcer strain, HP250. It
contained 1,821 bp, predicting 606 amino acids and had 95.7 ﹪, 94.8 ﹪and
97.9 ﹪, 98.0 ﹪identity with H. pylori 26695 and H. pylori J99, respectively.
Isogenic flgK mutant was constructed by disruption of the flgK gene with a
chloramphenicol resistance cassette using the allelic-exchange technique. The
mutation was confirmed by Southern blot and Western blot analyse. No
significant difference of urease activity was found between the wild-type and
mutant strains. For the wild-type strain, the typical sheathed flagella were
observed by electron microscopy and the large spread halos surrounding the
colony was detected in semisolid media. In contrast, no flagellar filaments
and the defect in motility were observed with the mutant strain. No significant
difference between the wild-type and mutant strains in adherence to the AGS
cells. However, the wild-type strain showed heavier density colonization and
more severe gastritis than the mutant strain in BALB/c mice. These results
demonstrate that the flgK gene is an essential element in the assembly of
functional flagella and is involved in colonization of H. pylori in the gastric
mucosa in BALB/c mice.

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