How much tissue is in the human body

We wished to incorporate the dermal thickness d into the calculation. Dermal thickness was directly measured at 17 locations throughout the body [ 34 ], with the mean of these measurements yielding 0. Combining these we find: N der. Our revised calculations of the number of glial cells, endothelial cells, and dermal fibroblast yield only 0. This leaves us with 3. We note that the uncertainty and CV estimates might be too optimistically low, as they are dominated by the reported high confidence of studies dealing with red blood cells but may underestimate systematic errors, omissions of some cell types, and similar factors that are hard to quantify.

In Fig 2 , we summarize the revised results for the contribution of the different cell types to the total number of human cells. This is the subject of the following analysis. Representation as a Voronoi tree map where polygon area is proportional to the number of cells. It is prudent in making such estimates to approach the analysis from different angles.

In that spirit, we now ask does the cumulative mass of the cells counted fall within the expected range for a reference adult? To properly tackle that question, we first need to state what the anticipated result is, i. A comprehensive systematic source for the composition of total cell mass rather than total cell count is the Report of the Task Group on Reference Man [ 6 ], which gives values for the mass of the main tissues of the human body.

This mass per tissue analysis includes both intra- and extracellular components. To distinguish between intra- and extracellular portions of each tissue, we can leverage total body potassium measurements [ 38 ] as detailed in S1 Appendix. Fig 3 compares the main tissues that contribute to the human body, in terms of cell number and masses.

For comparison, the contribution of bacteria is shown on the right, amounting to only 0. A striking outcome of this juxtaposition is the evident discordance between contributors to total cell mass and to cell number.

At the other extreme, bacteria have a minor contribution in terms of mass, but a cell count comparable to all human cells combined, as discussed above. The mass balance accounts well for all expected body mass, giving support to our analysis.

The option of overlooking a collection of very small cells numerous enough to alter the total cell count is further discussed in the S1 Appendix. With the revised estimates for the number of human 3.

We note that if one chooses to compare the number of bacteria in the human body 3. This is because the dominant population of non-nucleated red blood cells is not included in the calculation. We note that this ratio is the result of both the number of bacteria and the number of nucleated human cells in the body being several times lower than in the original s estimate that did not restrict the analysis to nucleated cells. We view red blood cells as bona fide cells, as their name suggests. Indeed, this opens an interesting tangential discussion on what should be defined as a cell.

Looking at our estimate, we identify four main parameters that dominate the calculation:. These are the governing parameters due to the dominating contribution of the colonic bacteria and RBC count to the total bacterial and human cell counts, respectively. Table 3 collects the changes to each of the previously mentioned parameters for individuals that represent different segments of the human population: reference adult woman 1.

Review of the literature shows no significant effect on the colonic bacterial concentrations over age from the one month old infant to the elderly [ 40 , 41 ]. As with age, extremes of weight have low impact on bacterial cell counts. We note that additional factors such as race and ethnicity may influence the B:H ratio. It has been shown that the bacterial population in the colon is strongly affected by geography [ 47 ], but current data is not enough to allow robust inference for the colonic concentrations and represents a data gap.

In this study, beyond providing up-to-date estimates on the average values of the number of cells, we aimed to give representative uncertainty ranges and the variation across population segments. This is based on comparing independent studies and the variation observed within studies.

The biggest knowledge gap we find is how realistic is the usage of the measured fecal bacteria density to represent also the average bacteria density in the colon. The change in bacteria concentration arises from several factors, including water absorption that concentrates the bacteria in the colon, as well as from bacteria growth during the 1—2 day transit time and the shedding of bacteria from the mucosal surface.

In some respects, the estimate we performed of multiplying observed fecal bacteria density with colon content volume can be considered an upper limit. More information on the relation between the actual densities of bacteria throughout the colon and those densities measured in feces will be a big step forward in improving the estimates of this study.

Another element of uncertainty is the limited information on the volume of the colon content across individuals and conditions. These knowledge gaps indicate that there might be systematic errors beyond what we could account for in the uncertainty ranges we report. In analyzing various population segments, our paper is clearly limited in scope.

We touched on the obese, neonate, and elderly as well as the effect of gender but have not dealt with many other segments of interest, such as individuals in the course of antibiotic treatment or bowel preparation for colonoscopy, people with infections, chronic diseases of the GI tract, etc. While we analyzed cell numbers, many researchers are interested in the number of genes as a reflection, for example, of the diversity of the microbiome metabolic capabilities.

In order to properly estimate by what factor the genes in the bacteria we harbor outnumber our own twenty thousand genes, the very delicate question of what should be considered different genes must be properly defined, which is beyond the scope of this study. We note in passing that the number of endosymbiotic bacteria that we harbor in the form of mitochondria probably outnumbers the body bacteria several fold.

This can be appreciated by noting that most cell types though not red blood cells contain hundreds or more of mitochondria per cell [ 48 ]. Should we care about the absolute number of human cells in the body or the ratio of bacterial to human cells? Updating the ratio of bacteria to human cells from or to closer to does not take away from the biological importance of the microbiota. Yet, we are convinced that a number widely stated should be based on the best available data, serving to keep the quantitative biological discourse rigorous.

The study of absolute numbers is also of relevance for specific biological questions. For example, a recent study showed how knowing the number of cells in different tissues can be an important indicator in understanding variation in cancer risk among tissues [ 49 ]. Other applications refer to the dynamic processes of development and mutation accumulation.

Finally, the type of numeric focus exercised here reveals and attracts attention to knowledge gaps such as the bacterial population densities in the proximal colon and how well are they represented by current analysis methods. Spreadsheets with the detailed calculations mentioned throughout the text and references for all data sources. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

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Elaboration of calculation methods and sanity check. S1 Data: Detailed calculations. Abstract Reported values in the literature on the number of cells in the body differ by orders of magnitude and are very seldom supported by any measurements or calculations. Introduction How many cells are there in the human body? Results Origin of Prevalent Claims in the Literature on the Number of Bacterial Cells in Humans Microbes are found throughout the human body, mainly on the external and internal surfaces, including the gastrointestinal tract, skin, saliva, oral mucosa, and conjunctiva.

Distribution of Bacteria in Different Human Organs Table 1 shows typical order of magnitude estimates for the number of bacteria that reside in different organs in the human body. Table 1 Bounds for bacteria number in different organs, derived from bacterial concentrations and volume.

Open in a separate window. Box 1. The Total Number of Bacteria in the Body We are now able to repeat the original calculation for the number of bacteria in the colon [ 3 ].

Concentration of Bacteria in the Colon The most widely used approach for measuring the bacterial cell density in the colon is by examining bacteria content in stool samples.

Table 2 Values of bacteria density in stool as reported in several past articles. Apocrine secretion occurs when secretions accumulate near the apical portion of a secretory cell. That portion of the cell and its secretory contents pinch off from the cell and are released. The sweat glands of the armpit are classified as apocrine glands.

Like merocrine glands, apocrine glands continue to produce and secrete their contents with little damage caused to the cell because the nucleus and golgi regions remain intact after the secretory event. In contrast, the process of holocrine secretion involves the rupture and destruction of the entire gland cell.

The cell accumulates its secretory products and releases them only when the cell bursts. New gland cells differentiate from cells in the surrounding tissue to replace those lost by secretion.

The sebaceous glands that produce the oils on the skin and hair are an example of a holocrine glands Figure 4. Glands are also named based on the products they produce. A serous gland produces watery, blood-plasma-like secretions rich in enzymes, whereas a mucous gland releases a more viscous product rich in the glycoprotein mucin. Both serous and mucous secretions are common in the salivary glands of the digestive system.

Such glands releasing both serous and mucous secretions are often referred to as seromucous glands. In epithelial tissue, cells are closely packed with little or no extracellular matrix except for the basal lamina that separates the epithelium from underlying tissue. The main functions of epithelia are protection from the environment, coverage, secretion and excretion, absorption, and filtration. Cells are bound together by tight junctions that form an impermeable barrier.

They can also be connected by gap junctions, which allow free exchange of soluble molecules between cells, and anchoring junctions, which attach cell to cell or cell to matrix. The different types of epithelial tissues are characterized by their cellular shapes and arrangements: squamous, cuboidal, or columnar epithelia. Single cell layers form simple epithelia, whereas stacked cells form stratified epithelia. Very few capillaries penetrate these tissues.

Glands are secretory tissues and organs that are derived from epithelial tissues. Exocrine glands release their products through ducts. Endocrine glands secrete hormones directly into the interstitial fluid and blood stream.

Glands are classified both according to the type of secretion and by their structure. Merocrine glands secrete products as they are synthesized. Apocrine glands release secretions by pinching off the apical portion of the cell, whereas holocrine gland cells store their secretions until they rupture and release their contents.

In this case, the cell becomes part of the secretion. The structure of a tissue usually is optimized for its function. Describe how the structure of individual cells and tissue arrangement of the intestine lining matches its main function, to absorb nutrients. Columnar epithelia, which form the lining of the digestive tract, can be either simple or stratified.

The cells are long and narrow. The nucleus is elongated and located on the basal side of the cell. Ciliated columnar epithelium is composed of simple columnar epithelial cells that display cilia on their apical surfaces.

Skip to content Learning Objectives Describe the structural characteristics of the various epithelial tissues and how these characteristics enable their functions. By the end of this section, you will be able to: Explain the general structure and function of epithelial tissue Distinguish between tight junctions, anchoring junctions, and gap junctions Distinguish between simple epithelia and stratified epithelia, as well as between squamous, cuboidal, and columnar epithelia Describe the structure and function of endocrine and exocrine glands.

External Website Summary of Epithelial Tissue Cells Watch this video to find out more about the anatomy of epithelial tissues. External Website.

The complexity and stability of the microbial community are dependent on the specific characteristics of the skin site. This topographical and temporal survey provides a baseline for studies that examine the role of bacterial communities in disease states and the microbial interdependencies required to maintain healthy skin.

They find that the composition of virus populations inhabiting the tail ends of healthy intestines as represented in our stools is unique to each individual and stable over time.

BMC Genomics. Molecular analysis of the diversity of vaginal microbiota associated with bacterial vaginosis. However, little is known about the overall structure and composition of vaginal microbial communities; most of the earlier studies focused on predominant vaginal bacteria in the process of BV.

In the present study, the diversity and richness of vaginal microbiota in 50 BV positive and 50 healthy women from China were investigated using culture-independent PCR-denaturing gradient gel electrophoresis DGGE and barcoded pyrosequencing methods, and validated by quantitative PCR. RESULTS: Our data demonstrated that there was a profound shift in the absolute and relative abundances of bacterial species present in the vagina when comparing populations associated with healthy and diseased conditions.

In spite of significant interpersonal variations, the diversity of vaginal microbiota in the two groups could be clearly divided into two clusters. A total of , high quality pyrosequencing reads was obtained for evaluating bacterial diversity and 24, unique sequences represented all phylotypes.

The most predominant phyla of bacteria identified in the vagina belonged to Firmicutes, Bacteroidetes, Actinobacteria and Fusobacteria. The higher number of phylotypes in BV positive women over healthy is consistent with the results of previous studies and a large number of low-abundance taxa which were missed in previous studies were revealed.

These genera are potentially excellent markers and could be used as targets for clinical BV diagnosis by molecular approaches. The study also provides the most comprehensive picture of the vaginal community structure and the bacterial ecosystem, and significantly contributes to the current understanding of the etiology of BV. PMID: Infection of macrophages with mycobacteria has been shown to inhibit the macrophage response to IFN-gamma.

HDAC gene expression was not affected by mycobacterial infection. So what this is saying is that the mycobacteria are able to silence genes associated with the immune systems ability to react to infection by increasing HDAC. The use of HDAC inhibitors in culture lead to the clearance of recalcitrant intracellular bacterial infections. Its a Catch Joyce,Good point.

Helicobacter pylori were recently found circulating in peripheral blood, showing that the GI tract is not so well isolated from the rest of the body as had previously been believed. I think the gut flora is key to introduction of new species to our systemic intraphagocytic microbiota over time, and also to how much of the innate immune system is occupied keeping the 'nasties' at bay in the GI tract.

The interesting thing is that although the MP abx profoundly change the gut flora, they do not wipe it out - as can be seen when discontinuing abx, the flora repopulates fairly quickly. I did once hear a presentation where it was claimed that a course of Cipro wiped out gut flora for a year.

I don't believe that for a moment - the L-forms Difficult-to-culture bacteria that lack a cell wall and are not detectable by traditional culturing processes. Abstract Elucidating the biogeography of bacterial communities on the human body is critical for establishing healthy baselines from which to detect differences associated with diseases.

To obtain an integrated view of the spatial and temporal distribution of the human microbiota, we surveyed bacteria from up to 27 sites in seven to nine healthy adults on four occasions. We found that community composition was determined primarily by body habitat. Within habitats, interpersonal variability was high, whereas individuals exhibited minimal temporal variability.

Several skin locations harbored more diverse communities than the gut and mouth, and skin locations differed in their community assembly patterns.

These results indicate that our microbiota, although personalized, varies systematically across body habitats and time; such trends may ultimately reveal how microbiome changes cause or prevent disease. Tyers M, Mann M. Tremendous progress has been made in the past few years in generating large-scale data sets for protein-protein interactions, organelle composition, protein activity patterns and protein profiles in cancer patients.

But further technological improvements, organization of international proteomics projects and open access to results are needed for proteomics to fulfil its potential. Each edge in the graph represents an interaction between nodes, which are coloured according to Gene Ontology GO functional annotation.

Highly connected complexes within the data set, shown at the perimeter of the central mass, are built from nodes that share at least three interactions within other complex members.

The complete graph contains 4, nodes of 6, proteins encoded by the yeast genome, 12, interactions and an average connectivity of 2. The 20 highly connected complexes contain genes, 1, connections and an average connectivity of 5. We still don't understand what a very large proportion of our DNA actually does. Sure, we understand how the genes work, but genes make up far less than half the total size of a the human genome.

Well, a group at Oxford has started to hone in on one likely function: to perpetuate components of the Human Microbiome. Here is a simplified version of their hypothesis:.

This is an important concept, which I have touched upon a few times, but generally felt it too complex to explain in detail. Now this paper, and the two commentaries above, can help me communicate the concept. Our bodies are home to many times more bacterial cells than animal cells and countless trillions of viruses. Ancient retroviruses make up a good size chunk of our genome. Now, scientists have discovered that most any virus can set up shop in an animal's genomes and lay dormant for millions of years.

A complex relationship: the interaction among symbiotic microbes, invading pathogens, and their mammalian host. Topof page Abstract Symbiosis between microbes and their mammalian host is vital to maintaining homeostasis. Symbiotic microbes within the gastrointestinal tract provide an array of benefits to the host, including promotion of host immunity.

A coordinated effort of the host and symbiotic microbes deters the colonization and survival of many invading pathogens. However, pathogens have devised strategies to overcome these mechanisms. Furthermore, some pathogens can hijack host hormones and bacterial autoinducers to induce virulence traits. Insight into this communication will provide a foundation for the development of targeted antimicrobial therapies.

Most bacteria harbor toxin—antitoxin TA systems, in which a bacterial toxin is rendered inactive under resting conditions by its antitoxin counterpart. Under conditions of stress, however, the antitoxin is degraded, freeing the toxin to attack its host bacterium.

One such TA system, PezAT, has been difficult to study in the past because the PezT toxin is so toxic without its antitoxin counterpart that bacteria die before any useful measurements can be made. Here, we use a truncated version of PezT that kills bacteria more slowly than normal, allowing us to examine the mechanisms of how this TA system operates.

We find that zeta toxins convert an essential building block of bacterial cell walls known as UNAG into a form that prevents normal cell wall growth, causing distortions in bacterial shape that leave the bacteria vulnerable to the hydrostatic pressure of its contents. Consequently, the bacteria burst, similar to what happens when they are treated with penicillin. These results may serve useful for designing new antibiotics. Further details on connective tissue can be found in textbooks of histology and human anatomy.

Gartner, Leslie P. Color Textbook of Histology. Philadelphia, PA: W. Saunders, Co. Ross, Michael H. Romrell, and Gordon I. Histology: A Text and Atlas, 3rd ed. Saladin, Kenneth S.

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