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Analyzing commonly available and inexpensive immunomodulatory and anti-inflammatory medications to assess their possible effectiveness in improving the host response to COVID, this paper recommends the following: 1 optimize current health-cease reduce smoking, ensure adequate hypertension and diabetes control, continue exercising; 2 start on an HMG CoA reductase inhibitor "statin" for its immunomodulatory and anti-inflammatory properties, which may reduce the mortality associated with ARDS; and 3 consider using Diclofenac or other COX-2 inhibition medications for its anti-inflammatory and virus toxicity properties. The downsides to these recommended interventions are considered manageable at this stage of the pandemic. Please enable it to take advantage of the complete set of features!

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Scientific rationale for a bottom-up approach to target the host response in order to try and reduce the s presenting with adult respiratory distress syndrome associated with covid is there a role for statins and cox-2 inhibitors in the prevention and early treatment of the disease?

NCBI Bookshelf. Molecular Biology of the Cell. New York: Garland Science; We have just seen that pathogens constitute a diverse set of agents. There are correspondingly diverse ranges of mechanisms by which pathogens cause disease. But the survival and success of all pathogens require that they colonize the host, reach an appropriate niche, avoid host defenses, replicate, and exit the infected host to spread to an uninfected one.

In this sectionwe examine the common strategies that are used by many pathogens to accomplish these tasks.

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The first step in infection is for the pathogen to colonize the host. Most parts of the human body are well-protected from the environment by a thick and fairly tough covering of skin. The protective boundaries in some other human tissues eyes, nasal passages and respiratory tract, mouth and digestive tract, urinary tract, and female genital tract are less robust.

For example, in the lungs and small intestine where oxygen and nutrients, respectively, are absorbed from the environment, the barrier is just a single monolayer of epithelial cells. Skin and many other barrier epithelial surfaces are usually densely populated by normal flora.

Some bacterial and fungal pathogens also colonize these surfaces and attempt to outcompete the normal flora, but most of them as well as all viruses avoid such competition by crossing these barriers to gain access to unoccupied niches within the host.

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Wounds in barrier epithelia, including the skin, allow pathogens direct access to the interior of the host. This avenue of entry requires little in Bottom needs host way of specialization on the part of the pathogen. Indeed, many members of the normal flora can cause serious illness if they enter through such wounds.

Anaerobic bacteria of the genus Bacteroidesfor example, are carried as harmless flora at very high density in the large intestine, but they can cause life-threatening peritonitis if they enter the peritoneal cavity through a perforation in the intestine caused by trauma, surgery, or infection in the intestinal wall.

Staphylococcus from the skin and nose, or Streptococcus from the throat and mouth, are also responsible for many serious infections resulting from breaches in epithelial barriers. Dedicated pathogens, however, need not wait for a well-timed wound to allow them access to their host. A particularly efficient way for a pathogen to cross the skin is to catch a ride in the saliva of a biting insect. Many arthropods nourish themselves by sucking blood, and a diverse group of bacteria, viruses, and protozoa have developed the ability to survive in the arthropod so that they can use these biting animals as vectors to spread from one mammalian host to another.

As discussed earlier, the Plasmodium protozoan that causes malaria develops through several forms in its life cycle, including some that are specialized for survival in a human and some that are specialized for survival in a mosquito see Figure Viruses that are spread by insect bites include the causative agents for several types of hemorrhagic fever, including yellow fever and Dengue fever, as well as the causative agents for many kinds of viral encephalitis inflammation of the brain. All these viruses have acquired the ability to replicate in both insect cells and mammalian cells, as is required for a virus to be transmitted by an insect vector.

Bloodborne viruses such as HIV that are not capable of replicating in insect cells are rarely, if ever, spread from insect to human.

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The efficient spread of a pathogen via an insect vector requires that individual insects consume blood meals from numerous mammalian hosts. In a few striking cases, the pathogen appears to alter the behavior of the insect so that its transmission is more likely.

Like most animals, the tsetse fly whose bite spre the protozoan parasite Trypanosoma brucei which causes sleeping sickness in Africa stops eating when it is satiated. But tsetse flies carrying trypanosomes bite much more frequently and ingest more blood than do uninfected flies.

The presence of trypanosomes impairs the function of the insect mechanoreceptors that measure blood flow through the gullet to assess the fullness of the stomach, effectively fooling the tsetse fly into thinking that it is still hungry. The bacterium Yersinia pestiswhich causes bubonic plague, uses a different mechanism to ensure that a flea carrying it bites repeatedly: it multiplies in the flea's foregut to form aggregated masses that eventually enlarge and physically block the digestive tract.

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The insect is then unable to feed normally and begins to starve. During repeated attempts to satisfy its appetite, some of the bacteria in the foregut are flushed into the bite site, thus transmitting plague to a new host Figure The spread of plague. This micrograph shows the digestive tract dissected from a flea that had dined about two weeks ly on the blood of an animal infected with the plague bacterium, Yersinia pestis.

The bacteria multiplied in the flea gut to produce more Hitching a ride through the skin on an insect proboscis is just one strategy that pathogens use to pass through the initial barriers of host defense. Whereas many barrier zones such as the skin, mouth, and large intestine, are densely populated by normal flora, others including the lower lung, the small intestine, and the bladder, are normally kept nearly sterile, despite relatively direct access to the environment.

The epithelium in these zones actively resists bacterial colonization.

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As discussed in Chapter 22, the respiratory epithelium is covered with a layer of protective mucus, and the coordinated beating of cilia sweeps the mucus and trapped bacteria and debris up and out of the lung. The epithelia lining the bladder and the upper gastrointestinal tract also have a thick layer of mucus, and these organs are periodically flushed by micturition and peristalsis, respectively, to wash away undesirable microbes.

The pathogenic bacteria and parasites that infect these epithelial surfaces have specific mechanisms for overcoming these host cleaning mechanisms. Those that infect the urinary tract, for example, resist the washing action of urine by adhering tightly to the bladder epithelium via specific adhesinsproteins or protein complexes that recognize and bind to host cell-surface molecules.

An important group of adhesins in uropathogenic E. These surface projections can be several micrometers long and are thus able to span the thickness of the protective mucus layer. At the tip of each pilus is a protein that binds tightly to a particular disaccharide linked to a glycolipid that is found on the surface Bottom needs host cells in the bladder and kidney Figure Uropathogenic E. A Scanning electron micrograph of uropathogenic E. B A close-up view of the bacteria more One of the hardest organs for a microbe to colonize is the stomach. This extreme environment is lethal to almost all bacteria ingested in food.

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Nonetheless, it is colonized by the hardy and enterprising bacterium Helicobacter pyloriwhich was recognized only recently as a major causative agent of stomach ulcers and possibly stomach cancer. Although the older treatments for ulcers acid-reducing drugs and bland diets are still used to reduce inflammation, a short and relatively cheap course of antibiotics can now effectively cure a patient of recurrent stomach ulcers.

The hypothesis that stomach ulcers could be caused by a persistent bacterial infection of the stomach lining initially met with considerable skepticism.

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The point was finally proven by the young Australian doctor who made the initial discovery: he drank a flask of a pure culture of H. One way that H. The bacteria also express at least five types of adhesins, which enable them to adhere to the stomach epithelium, and they produce several cytotoxins that destroy the stomach epithelial cells, creating painful ulcers.

The resulting chronic inflammation promotes cell proliferation and thus predisposes the infected individual to stomach cancer. A more extreme example of active colonization is provided by Bordetella pertussisthe bacterium that causes whooping cough. The first step in a B. The bacteria circumvent the normal clearance mechanism the mucociliary escalator described in Chapter 22 by binding tightly to the surface of ciliated cells and multiplying on them. The adherent bacteria produce various toxins which eventually kill the ciliated cells, compromising the host's ability to clear the infection.

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The most familiar of these is pertussis toxinwhich—like cholera toxin—is an ADP-ribosylating enzyme. Not content with this, B. The bacterially-produced enzyme is therefore active only in the cytoplasm of a eucaryotic cell. Although both B. Not all examples of specific colonization require that the bacterium express adhesins that bind to host cell glycolipids or proteins.

Enteropathogenic E. After Tir is inserted into the host cell membranea bacterial surface protein binds to the extracellular domain of Tir, triggering a remarkable series of events inside the host cell.

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First, the Tir receptor protein is phosphorylated on tyrosine residues by a host protein tyrosine kinase. Unlike eucaryotic cells, bacteria generally do not phosphorylate tyrosine residues, yet Tir contains a peptide domain that is a specific recognition motif for a eucaryotic tyrosine kinase. The phosphorylated Tir then is thought to recruit a member of the Rho family of small GTPases, which promotes actin polymerization through a series of intermediate steps discussed in Chapter Interaction of enteropathogenic E.

Tir then inserts into more These examples of host colonization illustrate the importance of host- pathogen communication in the infection process. Pathogenic organisms have acquired genes that encode proteins that interact specifically with particular molecules of the host cells. In some cases, such as the B. Many pathogens, including V. Others, however, including all viruses and many bacteria and protozoaare intracellular pathogens.

Their preferred niche for replication and survival is within the cytoplasm or intracellular compartments of particular host cells. This strategy has several advantages.

The pathogens are not accessible to antibodies discussed in Chapter 24and they are not easy targets for phagocytic cells discussed below. This lifestyle, however, does require that the pathogen develop mechanisms for entering host cells, for finding a suitable subcellular niche where it can replicate, and for exiting the infected cell to spread the infection. In the remainder of this sectionwe consider some of the myriad ways that individual intracellular pathogens exploit and modify host cell biology to satisfy these requirements.

The first step for any intracellular pathogen is to bind to the surface of the host target cell. For viruses, binding is accomplished through the association of a viral surface protein with a specific receptor on the host cell surface. Of course, no host cell receptor evolved for the sole purpose of allowing a pathogen to bind to it; these receptors all have other functions.

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Its normal function is as a transport protein responsible for the uptake of maltose. Viruses that infect animal cells generally use cell-surface receptor molecules that are either very abundant such as sialic- acid -containing oligosaccharides, which are used by the influenza virus or uniquely found on those cell types in which the virus can replicate such as the nerve growth factor receptor, the nicotinic acetylcholine receptoror the cell-cell adhesion protein N-CAMall of which are used by the rabies virus to specifically infect neurons.

Often, a single type of receptor is used by many types of virus, and some viruses can use several different receptors.

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Moreover, different viruses that infect the same cell type may each use a different receptor. Hepatitis, for example, is caused by at least six viruses, all of which preferentially replicate in liver cells. Receptors for four of the hepatitis viruses have been identified, and they are all different.

Receptors need not be proteins; herpes simplex virus, for example, binds to heparan sulfate proteoglycans through specific viral membrane proteins. Frequently, viruses require both a primary receptor and a secondary co-receptor for efficient attachment and entry into host cells.

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