嗜中性粒细胞呈圆形，胞质淡红色。胞核幼稚型的呈杆状或马蹄形，成熟的呈分叶状，三叶的较多见，中性粒细胞来源于骨髓的造血干细胞，在骨髓中分化发育后，进入血液或组织。

中性粒细胞来源于骨髓的造血干细胞，在骨髓中分化发育后，进入血液或组织。在骨髓、血液和结缔组织的分布数量比是28：1：25，成年人血液中中性粒细胞的数量约占白细胞总数的55％一70％。中性粒细胞属多形核白细胞的一种，由于其数量在粒细胞中最多，因此有人将多形核白细胞指中性粒细胞。

该细胞内含许多弥散分布的细小的浅红或浅紫色的特有颗粒，颗粒中含有髓过氧化物酶、酸性磷酸酶、吞噬素、溶菌酶等。髓过氧化物酶是中性粒细胞所特有，即使在有强吞噬作用的巨噬细胞中也极少或完全没有这种酶。在细胞化学上，一般将这种髓过氧化物酶作为中性粒细胞的标志。中性粒细胞具有很强的趋化作用。所谓趋化作用，就是细胞向着某一化学物质刺激的方向移动。对中性粒细胞起趋化作用的物质，称为中性粒细胞趋化因子。中性粒细胞膜上有趋化因子受体，受体与趋化因子结合，激活胞膜上的钙泵，细胞向前方伸出片足，使细胞移向产生趋化因子的部位。

中性粒细胞的片足与产生趋化因子的异物接触后，接触处周围的胞质形成隆起即伪足，接触部位的细胞膜下凹，将异物包围，形成含有异物的吞噬体或吞噬泡。中性粒细胞膜表面有IgGFc受体和补体C3受体，可加速吞噬作用。被吞噬的异物裹有抗体和补体时，与中性粒细胞膜上的相应受体结合，而加强了细胞对它的吞噬作用，称为调理作用。

细胞随着吞噬作用的开始，导致细胞膜紊乱而引起呼吸爆发，细胞耗氧量增加，产生大量的过氧化物及超氧化物等细胞毒性效应分子，对寄生虫具有杀伤活性。在IFN-γ和TNF刺激下，则可产生更多的过氧代谢阴离子，杀死胞外寄生虫。中性粒细胞在杀死吞噬的细菌等异物后，本身也死亡，死亡的中性粒细胞称为脓细胞。

中性粒细胞受细菌产物、抗原抗体复合物等作用时，细胞的颗粒内容物向细胞外释放。释出的酸性蛋白酶和中性蛋白酶，可以分解血管基膜、肾小球基膜、结缔组织的胶原蛋白与弹性蛋白以及血浆中的补体C5、C15和激肽原等。其分解产物有的又是中性粒细跑趋化因子，能吸引更多的中性粒细胞。中性粒细胞释放的物质中，还有嗜酸性粒细胞趋化因子、中性粒细胞不动因子(NIF)、激肽酶原、血纤维蛋白溶酶原、凝血因子、白三烯等(成令忠，1993)。

除了在抗感染中起重要的防御作用外，中性粒细胞可引起感染部位的炎症反应并参与寄生虫感染引发的变态反应，从而引起免疫病理损害。抗体直接作用于组织或细胞上的抗原，中性粒细胞通过其Fc受体与靶细胞表面的IgGFc段结合，发挥ADCC作用，从而导致细胞毒型变态反应损害；当抗原抗体比例适合而形成19S大小的免疫复合物，不易被吞噬，沉积于毛细血管壁，激活补体，吸引中性粒细胞至局部。中性粒细胞通过Fc受体和C3b受体与免疫复合物结合并吞噬之。吞噬过程中脱颗粒，释放出一系列溶酶体酶类，造成血管和周围组织的损伤；在IgE介导的速发型变态反应的部位，也有中性粒细胞的聚集，说明中性粒细胞也参与了速发型变态反应导致的病理损害(刘约翰等，1993)。

推荐大家阅读一篇文献：Neutrophils: Molecules, Functions and Pathophysiological Aspects

全文下载地址：Neutrophils: Molecules, Functions and Pathophysiological Aspects

Biology of Disease

Lab Invest 2000, 80:617–653

Neutrophils: Molecules, Functions and Pathophysiological Aspects

Véronique Witko-Sarsat1, Philippe Rieu1, Béatrice Descamps-Latscha1, Philippe Lesavre1 and Lise Halbwachs-Mecarelli1

1INSERM U507, Necker Hospital, Paris, France

Correspondence: Dr. V. Witko-Sarsat, INSERM U507, Necker Hospital, 161, rue de Sèvres, 75015 Paris, France. Fax: 01 45 66 51 33; E-mail: witko-sarsat@necker.fr

Received 8 February 2000.

INTRODUCTION
I. NEUTROPHIL MOLECULES AND FUNCTIONS
I.A. ADHESION AND MIGRATION
I.A.1. Traffic and margination
I.A.2. Adhesion to the Endothelial Wall
Rolling and Tethering
Neutrophil Priming During Rolling
Firm Adhesion and Spreading
I.A.3 Extravasation and Diapedesis Toward Inflammatory Stimuli
Transendothelial Migration
Migration Within Interstitial Tissues
Signaling by Chemoattractants
Transepithelial Migration
I.B. PHAGOCYTOSIS, DEGRANULATION AND BACTERIA KILLING
I.B.1. Phagocytosis
I.B.2. Degranulation
Granule Biogenesis
Mechanisms of Degranulation
I.B.3. Microbicidal Molecules
NADPH-Derived Oxidants
The H2O2-Myeloperoxidase System
Nitric Oxide-Synthase-Derived Reactive Nitrogen Intermediates
Granule Proteins
Antimicrobial Proteins
Proteases
I.C. CYTOKINE SYNTHESIS
I.C.1. TNF- as a Proinflammatory Cytokine
I.C.2. IL-1 and IL-1 Receptor Antagonist (IL-1-Ra)
I.C.3. IL-8 as a Prototype of Chemokines
I.C.4. Modulation of Cytokine Expression by Neutrophils
IFN-
IL-10
IL-4 and IL-13
I.C.5. Molecular Regulation of Cytokine Production
I.D. APOPTOSIS AND RESOLUTION OF ACUTE INFLAMMATION
I.D.1. Progressive Decrease of Neutrophil Recruitment
I.D.2. Apoptosis in Resolution of Inflammation
II. NEUTROPHILS IN PATHOLOGY
II.A. Bacterial Infection
II.B. Tissue Injury-Induced Inflammation: Ischemia-Reperfusion Injury
II.C. Crystal-Induced Inflammation
II.D. Complement-Induced Inflammation and Oxidative Stress: Hemodialysis
II.E. Immune Complex-Induced Inflammation: Antibody-Mediated Glomerunephritis
II.F. Cytokine-Induced Inflammation: Rheumatoid Arthritis
II.G. Antineutrophil Cytoplasmic Antibodies and Vasculitis: Autoimmunity Against Neutrophil Components
II.H. Genetic Disorders of Neutrophil Regulations: Hereditary Periodic Fever Syndromes
II.I. Cystic Fibrosis: The Paradox of an Exacerbation of Neutrophil-Mediated Tissue Damage and a Concomitant Persistence of Infection
CONCLUSION
The notion that inflammation is the net resultant of pro and contra inflammatory pathways (Fauve, 1980) is well illustrated by the dual role of neutrophils which combine an anti-infectious and a proinflammatory role (Klebanoff, 1992; Ward, 1999; Weiss, 1989). The aim of this report is to review the main physiological and pathogenic activities of neutrophils—ie, adherence and migration, degranulation and release of inflammatory mediators, phagocytosis and apoptosis—in the light of the most recent molecular data on extracellular effectors and regulators, membrane receptors, and intracellular signaling pathways involved in these functions.

Leukocyte adhesion processes have been studied extensively during the last decade and most membrane molecules responsible for leukocyte interactions with other cells or with the extracellular matrix have been identified. New data are constantly reported on sophisticated intracellular pathways that allow neutrophils to integrate signals transmitted by adhesion partners with those of chemoattractants and cytokines. What remains puzzling is that leukocytes mostly use the same adhesion molecules to adhere to inflamed endothelium, as do lymphocytes to constantly recirculate from the blood to lymphoid tissues. Still, naive lymphocytes are the only leukocytes to cross endothelia of lymphoid high endothelial venules, while neutrophils are the first leukocytes, hours before monocytes or lymphocytes, to migrate specifically across the endothelium adjacent to the inflammation site. The selectivity and specific timing of such a highly redundant system is just becoming comprehensible, in particular with the description of the chemokine and serpentine families.

Another aspect reviewed here is the wide variety of effector molecules required to achieve the usual microbicidal role of neutrophils, including radical oxygen species (ROS), proteinases, bactericidal proteins and cytokines, which either alone or in concert may interact in up- or down-regulating the major inflammatory processes. We emphasize new directions of investigation regarding these neutrophil-derived effector molecules, as exemplified by myeloperoxidase-derived oxidants whose implications go far beyond inflammatory diseases. The potential clinical use of neutrophil-derived antibiotic proteins is illustrated by the Bactericidal Permeability Increasing protein (BPI), now undergoing clinical trials, and the design of novel antimicrobial peptides based on studies on defensins and cathelicidins.

Finally, we illustrate the various aspects of neutrophil biology by classifying, according to their predominant neutrophil-activating mechanism, diseases in which neutrophils play a pivotal role. Comprehension of the activation pathways will allow us to analyze, and possibly prevent, chronic inflammation processes where dysregulated neutrophil recruitment and activation results in severe damage of adjacent normal tissues.