Complication of sinusitis:
Paranasal sinusitis can have devastating intracranial sequelae on rare conditions. Involvement of the adjacent pituitary gland and cavernous sinuses can result in serious neurological morbidity or mortality, and retrograde spread of infection through the basal venous system can result in subdural or parenchymal brain involvement. A high index of suspicion and aggressive medical and surgical treatment are crucial for patient survival, but the morbidity rate remains high (6). 

Intractable meningitis, intracranial abscess or cavernous sinus thrombosis could happen as a complication in a diabetic patient, arising from sphenoid sinusitis (7). 

Risk Factors:
Many of the risk factors are associated with exposure to contaminants, or activities that could lead to potential vulnerabilities in the immune system. 
 

Smoking.
Exposure to others in public places.
Illness that has lowered resistance.
Exposure to cold, damp weather outdoors or dry heat indoors.
Excessive nose blowing during an upper-respiratory infection.
Hard sneezing with the mouth closed.
Swimming in contaminated water, especially jumping into the water without holding the nose.
Abscess in an upper tooth.
Immunosuppression, as in people who have organ transplants and are taking drugs to suppress the immune function to prevent rejection.
Continuous positive airway pressure - used in obstructive sleep apnea to keep the upper airways open during sleep.
Air travel during upper respiratory infection.

 

It is important to stay aware of the environmental and behavioral triggers that can lead to this condition in order to prevent the recurrence of sinusitis.

Children have immature immune systems and are more prone to infections of the nose, sinus, and ears, especially in the first several years of life. These are most frequently caused by viral infections (colds), and they may be aggravated by allergies. Infection of the adenoid tissue, called adenoiditis, could cause obstruction of the back of the nose and can cause many of the symptoms that are similar to sinusitis, namely, runny nose, stuffy nose, post-nasal drip, bad breath, cough, and headache. If the child remains ill beyond the usual week to ten days, a serious sinus infection is likely. 

The risk of sinus infections could be reduced by reducing the exposure of children to known environmental allergies and pollutants such as tobacco smoke, reducing his/her time at day care, and treating stomach acid reflux disease. 

By distinguishing whether sinusitis is acute, recurrent, or chronic, the physician can determine the predisposing causes. Acute sinusitis is a frequent complication of a viral infection of the upper respiratory tract while recurrent and chronic sinusitis can result from anatomic abnormalities (some of which were previously described) and Immunological problems, most frequently allergic rhinitis. Other disorders such as humoral immunodeficiency are infrequently the cause, although they must be considered in the presence of other systemic infections or in patients whose condition fails to improve despite adequate therapy. Immotile cilia syndrome and cystic fibrosis are other possible etiologic factors. 

Common Etiological Factors of Sinusitis:

Viral infection, such as the common cold, flu: In these cases the body reacts by producing mucus and sending whit blood cells to the lining of the nose, which congest and swell the nasal passages. When this swelling involves the adjacent mucous membranes of the sinuses, air and mucus are trapped behind the narrowed opening of the sinuses. 

Bacteria infection: Some bacterial strains are normal inhabitant of the upper respiratory tract e.g. Streptococcus pneumoniae and Haemophilus influenzae. These bacteria have no ill effects until the body's defenses are weakened or drainage from the sinuses is blocked by a cold or other viral infection then they start to be virulent and cause infection of the upper respiratory tract and secondary sinusitis.

Fungal infections: Although fungi are abundant in the environment, they are usually harmless to healthy people, indicating that the human body has a natural resistance to them. Fungi, such as Aspergillus, cause serious illness in people whose immune systems are not functioning properly. Some people with fungal sinusitis have an allergic-type reaction to the fungi.

Allergic rhinitis: Inhalation of airborne allergens (substances that provoke an allergic reaction), such as dust, mold, and pollen, often set off allergic reactions (allergic rhinitis) that, in turn, may contribute to sinusitis. Hay fever may also be complicated by episodes of acute sinusitis. Patients with allergic rhinitis also often have chronic sinusitis. 

Vasomotor rhinitis, caused by humidity, cold air, alcohol, perfumes, and other environmental conditions, also may be complicated by sinus infections.

Immune deficiencies and HIV infection: Those patients are more susceptible to develop acute sinusitis than general population.

Cystic fibrosis and diseases of abnormal cilia: Acute and chronic sinusitis could happen as a result of abnormal mucus secretion or cilia movement. 

Deviated nasal septum or other obstruction of the nose due to nasal polyps may trap fluid in the sinuses. 

Aging rhinitis: As one ages, the nasal mucus loses its water content and becomes increasingly thick and sticky. Patients complain of post-nasal drip, cough, and hoarseness; the condition is best treated with nasal irrigation and increased hydration. 

Tumors: The presence of tumors in the sinuses is relatively uncommon. They are discovered with a nasal obstruction, often with heavy nosebleeds.

 The Role of The Immune System in Viral Infection and Allergic Disorders Of The Upper Respiratory Tract

In order to understand the role of the immune system in viral infection and allergic disorders of the upper respiratory tract, one should be acquainted with the component of the immune system and how each of the components works. 

The Immune System
The organs of the immune system are stationed throughout the body. They are generally referred to as the lymphoid organs because they are concerned with the development, growth and deployment of lymphocytes, the white cells that are the key operatives of the immune system.

Lymphoid organs include the bone marrow and the thymus as well as lymph nodes, spleen, tonsils and adenoids, the appendix, and clumps of lymphoid tissue in the small intestine known as Peyer's patches. The blood and lymphatic vessels that carry lymphocytes to and from the other structures can also be considered lymphoid organs. 

Cells destined to become immune cells, like all other blood cells, are produced in the bone marrow, the soft tissue in the hollow shafts of long bones (stem cells). The descendants of some so-called stem cells become lymphocytes, while others develop into a second major group of immune cells typified by the large, cell-and particle-devouring white cells known as phagocytes. 

The two major classes of lymphocytes are: 

B cells complete their maturation in the bone marrow and become capable of being transformed into plasma cells upon contact with the antigen to produce the antibodies. 

T cells, on the other hand, migrate to the thymus, a multi-lobed organ that lies high behind the breastbone. There they multiply and mature into cells capable of producing immune response and become immunocompetent. In a process referred to as T cell "education," T cells in the thymus learn to distinguish self- cells from non-self cells; T cells that would react against self-antigens are normally eliminated. 

Upon exiting the bone marrow and thymus, some lymphocytes congregate in immune organs or lymph nodes. Others-both B and T cells-travel widely and continuously throughout the body. They use the blood circulation as well as a body-wide network of lymphatic vessels similar to blood vessels. 


The Lymphoid Organs



The lymph nodes: They are small bean-shaped bodies in the form of clusters in the neck, armpits, abdomen, and groin. Each lymph node contains specialized compartments that house platoons of B-lymphocytes, T lymphocytes, and other cells capable of enmeshing antigen and presenting it to T cells. Thus, the lymph node brings together the several components needed to spark an immune response. 

The spleen, too, provides a meeting ground for immune defenses. Like the lymph nodes, the spleen's lymphoid tissue is subdivided into compartments that specialize in different kinds of immune cells. Microorganisms carried by the blood into the spleen become trapped by the immune cells known as macrophages. (Although people can live without a spleen, persons whose spleens have been damaged by trauma or by disease such as sickle cell anemia are highly susceptible to infection). 

Clusters of lymphoid tissue are found in many parts of the body. They are common around the mucous membranes lining the respiratory and digestive tracts-areas that serve as gateways to the body. They include the tonsils and adenoids, the appendix, and Peyer's patches. 

The lymphatic vessels carry the lymph, which transport a mix of lymphocytes, macrophages, and foreign antigens to lymph nodes, where antigens can be filtered out and presented to immune cells. 

Additional lymphocytes reach the lymph nodes (and other immune tissues) through the bloodstream. An artery and a vein supply each node; lymphocytes enter the node by traversing the walls of the very small, specialized veins. 
All lymphocytes exit lymph nodes in lymph via outgoing lymphatic vessels. At the base of the neck, large lymphatic vessels merge into the thoracic duct, which empties its contents into the bloodstream. 

Once in the bloodstream, the lymphocytes and other assorted immune cells are transported to tissues throughout the body. They patrol everywhere for foreign antigens, then gradually drift back into the lymphatic vessels, to begin the cycle all over again. 

Antiviral Immunity
Viruses are small, obligate intracellular parasites, which cause infection by invading cells of the body and multiplying within them. Within their life cycle they have a relatively short extracellular period, prior to infecting the cells, and a longer intracellular period during which they undergo replication. Cold virus particles, once they slip into cells of the upper respiratory tract, start copying themselves. To defend itself, the immune system pumps out chemicals called cytokines. Two of these cytokines in particular contribute to the sore throat, sneezing, and runny nose of a cold. The lecture will describe the effector mechanisms, which the immune response uses to combat viral infections, and will then place these mechanisms in the context of acute infection with influenza virus.

The immune system has mechanisms which can attack the virus in both phases of its life cycle (extracellular and intracellular phases), and which involve both non-specific and specific effector mechanisms.

Non-Specific Mechanisms
Interferons: 
Viral infection of cells directly stimulates the production of interferons (note that the "type 1" interferons which are produced non-specifically by many cell types in response to viral infection are quite distinct from the T cell cytokine gamma interferon which is produced by CD4+ and CD8+ T cells in response to antigenic stimulation). 

Interferon type 1 function
Type I interferons lead to the induction of an "antiviral state" in the cells, which is characterized by inhibition of both viral replication and cell proliferation, and also enhancement of the ability of natural killer cells to lyse virally infected cells. Indeed, the interferons may be among the most broadly active of all the immunologic and physiologic regulators. 

Natural Killer Cells:
NK cells possess the ability to recognize and lyse virally infected cells and certain tumor cells. Whilst not showing antigen specificity, they clearly exhibit some degree of selectivity in targeting "abnormal" cells for lysis (8,9). The main advantage that NK cells have over antigen-specific lymphocytes in antiviral immunity is that there is no "lag" phase of clonal expansion for NK cells to be active as effectors, as there is with antigen-specific T and B lymphocytes. Thus NK cells may be effective early in the course of viral infection, and may limit the spread of infection during this early stage, while antigen-specific lymphocytes are being recruited and clonally expanded. 

Specific Mechanisms
Both cell mediated and humoral arms of the immune response play a role as specific effector mechanisms in antiviral immunity. 

1. Cell Mediated Immunity (T Cells and Cytokines)
T- cells:
T-cells contribute to the immune defenses in two major ways. 
Regulatory T cells are vital to orchestrating the elaborate system. (B cells, for instance, cannot make antibody against most substances without T cell help).

There are two types of regulatory cells:
T-cells contribute to the immune defenses in two major ways. 
 

Helper T cells, which are typically identifiable by the T 4-cell marker, and are essential for activating B cells and other T cells as well as natural killer cells and macrophages.
Suppressive T cells which release suppressive cytokines, such as TGF-b, IL-4 and IL-10 to down-regulate or suppress the immune response and keep it from going out of control by turning the helper cells off (10).

 

Cytotoxic T cells, (or "killer") T cells: They aggressively screen other cells for signs of infection and malignancy and secrete toxic molecules to kill any aberrant cells, thus ridding the body of cells that have been infected by viruses or transformed by cancer. They usually carry the T8 marker.


Cytokines
T cells work primarily by secreting substances known as cytokines that include Lymphokines (which are also secreted by B cells) and their relatives, and the monokines produced by monocytes and macrophages. Both types are diverse and potent chemical messengers.

Mature T cells
Cytokine secretion

Cytokine function: A single cytokine may have many functions; conversely, several different cytokines may be able to produce the same effect. 
 

Binding to specific receptors on target cells, Lymphokines call into play many other cells and substances, including the elements of the inflammatory response. 
They encourage cell growth, promote cell activation, direct cellular traffic, destroy target cells, and incite macrophages. 

 

Cytokines include the following types:
 

1.  Interferons: It is one of the first cytokines to be discovered. It is produced by T cells and macrophages (as well as by cells outside the immune system), interferons are a family of proteins with antiviral properties. Interferon from immune cells, known as immune interferon or gamma interferon, activates macrophages. The IFN- appearing early in the infection probably arises from natural killer (NK) cells, whereas that occurring later in a more sustained lower respiratory infection would more likely arise from T cells mediating the Th1 (helper T cells) response necessary for effective resolution of the infection. 
2. Tumor Necrosis Factor alpha TNFalpha: It is made by many different cells including neutrophils, lymphocytes and Natural Killer (NK) cells. 
TNF alpha function:
TNFalpha initiates a cascade of cytokines, which mediate an inflammatory response. 
TNFalpha regulates the expression of many genes important for the host response to infection. 
3. Transforming Growth Factor-b (TGF-beta): It is found at highest concentration in platelets. 
TGF-beta function
It stimulates macrophage secretion of various growth factors. 
It inhibits activated macrophage production of reactive oxygen and reactive nitrogen metabolites.
4. Macrophage Colony Stimulating Factor (M-CSF): It is produced by many cells including macrophages themselves. 
M-CSF function
It is important for the survival, proliferation and differentiation of monocytes, macrophages.
It is responsible for the upregulation of Macrophage Scavenger Receptor activity. 
5. Interleukins: They are considered as messengers between leukocytes, or white cells. They were initially given descriptive names but, as their basic structure has been identified they are named as intereukins and they include the following types: 
IL-1beta: It is a pro-inflammatory cytokine, which is secreted by macrophages activated by a number of stimuli including TNFalpha, bacterial endotoxin and IL-1beta itself. It exerts its effects on many different cell types locally at the site of production and systemically (at a distance) and attract different types of granulocytes and help their degranulation releasing their chemicals which causes the different disease symptoms. 
IL-2, originally known as T cell growth factor, TCGF, is produced by antigen-activated T cells and promotes the rapid growth or differentiation of mature T cells and B cells. 
IL-3, is a T-cell derived member of the family of protein mediators known as colony-stimulating factors (CSF); one of its many functions is to nurture the development of immature precursor cells into a variety of mature blood cells.
IL-4, IL-5, and IL-6 help B cells grow and differentiate; IL-4 also affects T cells, macrophages, mast cells and granulocytes. IL-6 stimulates B-lymphocytes to produce antibodies and in concert with IL-1 causes T-cell activation.
IL-10: It is an immunoregulatory cytokine, which can exert a wide range of different effects on different cell types. It suppresses IL-2 by helper T-cells and thus keep the immune response from going out of control and stop inflammatory fulmination. It is also a potent modulator of monocyte/macrophage function.
IL-12: It stimulates growth of activated Natural killer cells, CD8+ and CD4+ T- cells. Activate the T helper cell response and increase the production of tumor necrosis factor (TNF) by macrophage cells. It also suppresses IL-4 induced IgE production.
IL-13: Interleukin 13 has very similar biological effects on macrophages to IL-4. 

 

  • March 06, 2015
  • DermaMed Pharmaceutical Inc.

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