A blood smear showing a Neutrophil Granulocyte; the three-lobulated nucleus can be seen. This picture has been stained with MayGrunwald Giemsa, and observed with a 1000x objective in oil immersion.
'Neutrophil granulocytes', generally referred to as ''neutrophils'', are the most abundant type of
white blood cells and form an integral part of the
immune system. Their name arrives from staining characteristics on
hematoxylin and
eosin (H&E) histological preparations. Whereas basophilic cellular components stain dark blue and eosinophilic components stain bright red, neutrophilic components stain a neutral pink. These
phagocytes are normally found in the
blood stream. However, during the
acute phase of
inflammation, particularly as a result of
bacterial
infection, neutrophils leave the vasculature and migrate toward the site of inflammation in a process called
chemotaxis. They are the predominant cells in
pus, accounting for its whitish/yellowish appearance. Neutrophils react within an hour of tissue injury and are the hallmark of acute inflammation.
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Measurement of neutrophils
Neutrophil granulocyte migrates from the blood vessel to the matrix, sensing proteolytic enzymes, in order to determine intercellular connections (to the improvement of its mobility) and envelop bacteria through phagocytosis.
Neutrophil granulocytes have an average volume of 330 femtoliters (fl) and a diameter of 12-15
micrometers (µm) in
peripheral blood smears.
With the
eosinophil and the
basophil, they form the class of ''polymorphonuclear cells'' (PMNs), named for the
nucleus's characteristic multilobulated shape (as compared to
lymphocytes and
monocytes, the other types of white cells). Neutrophils are the most abundant white blood cells; they account for 70% of all white blood cells (leukocytes).
The stated normal range for blood counts varies between laboratories, but a neutrophil count of 2.5-7.5 x 10
9/L is a standard normal range. People of African and Middle Eastern descent may have lower counts which are still normal.
Lifespan
The average halflife of a non-activated neutrophil in the circulation is about 4-10 hours. Upon activation, they marginate (position themselves adjacent to the blood vessel endothelium), undergo
selectin dependent capture followed by
integrin dependent adhesion after which they migrate into tissues, where they survive for 1-2 days.
Neutrophils are much more numerous than the longer-lived
monocyte/macrophages. The first phagocyte a
pathogen (disease-causing microorganism) is likely to encounter is a neutrophil. Some experts feel that the short lifetime of neutrophils is an
evolutionary adaptation to minimize propagation of those pathogens that
parasitize phagocytes. The more time such parasites spend outside a host
cell, the more likely they will be destroyed by some component of the body's defenses. However, because neutrophil
antimicrobial products can also damage host
tissues, other authorities feel that their short life is an adaptation to limit damage to the host during
inflammation.
Chemotaxis
Neutrophils undergo a process called
chemotaxis that allows them to migrate toward sites of infection or inflammation. Cell surface receptors are able to detect chemical gradients of molecules such as
interleukin-8 (IL-8),
interferon gamma (IFN-gamma), and
C5a which these cells use to direct the path of their migration.
Function
Neutrophil
Being highly
motile, neutrophils quickly congregate at a focus of
infection, attracted by
cytokines expressed by activated
endothelium,
mast cells and
macrophages.
Phagocytosis
Neutrophils are phagocytes, capable of ingesting microorganisms or particles. They can internalise and kill many microbes, each phagocytic event resulting in the formation of a phagosome into which
reactive oxygen species and hydrolytic enzymes are secreted. The consumption of oxygen during the generation of reactive oxygen species has been termed the "
respiratory burst," although it actually has nothing to do with respiration or energy production.
The respiratory burst involves the activation of the
enzyme NADPH oxidase, which produces large quantities of
superoxide, a reactive oxygen species. Superoxide dismutates, spontaneously or through catalysis via the enzyme
catalase, to hydrogen peroxide, which is then converted to
hypochlorous acid (HOCl, also known as chlorine bleach) by the green heme enzyme
myeloperoxidase. It is thought that the bactericidal properties of HOCl are enough to kill bacteria phagocytosed by the neutrophil, but this has not been proven conclusively.
Degranulation
Neutrophils also release an assortment of proteins in three types of granules by a process called
degranulation:
NETs
There is controversy about whether neutrophils can also extrude
neutrophil extracellular traps (NETs), a web of fibers composed of
chromatin and
serine proteases that trap and kill microbes extracellularly. It is suggested that NETs provide a high local concentration of antimicrobial components and bind, disarm, and kill microbes independent of phagocytic uptake. In addition to their possible antimicrobial properties, NETs may serve as a physical barrier that prevents further spread of pathogens. Recently, NETs have been shown to play a role in inflammatory diseases, as NETs could be detected in
preeclampsia, a pregnancy related inflammatory disorder in which neutrophils are known to be activated.
Role in disease
Low neutrophil counts are termed "
neutropenia". This can be
congenital (
genetic disorder) or it can develop later, as in the case of
aplastic anemia or some kinds of
leukemia. It can also be a
side-effect of
medication, most prominently
chemotherapy. Neutropenia predisposes heavily for infection. Finally, neutropenia can be the result of colonization by intracellular neutrophilic parasites.
Functional disorders of neutrophils are often hereditary. They are disorders of
phagocytosis or deficiencies in the
respiratory burst (as in
chronic granulomatous disease, a
rare immune deficiency, and
myeloperoxidase deficiency).
In
alpha 1-antitrypsin deficiency, the important neutrophil enzyme
elastase is not adequately inhibited by
alpha 1-antitrypsin, leading to excessive tissue damage in the presence of inflammation - most prominently
pulmonary emphysema.
In
Familial Mediterranean fever (FMF), a mutation in the ''pyrin'' (or ''
marenostrin'') gene, which is expressed mainly in neutrophil granulocytes, leads to a constitutionally active
acute phase response and causes attacks of
fever,
arthralgia,
peritonitis and - eventually -
amyloidosis.
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